CALA 2022 Friday Happy Hour Series
Ke Yuan
Jan 21st, 2022
Time: EST 10:30 am; PST: 7:30 am; Beijing time: 10:30pm
Zoom: 82407021221 (Password: 654321)
Reduced Notch1 Cleavage Promotes the Development of Pulmonary Hypertension
Jinjiang Pang, MD & PhD
Associate Professor
Aab Cardiovascular Research Institute, University of Rochester
Bio: Dr. Pang obtained her MD and PhD in China and completed her postdoctoral training with Dr. William Chilian and Dr. Bradford Berk who are the pioneers of cardiovascular field. Dr. Pang’s research is mainly focused on angiogenesis and vascular remodeling, which are critical events for tissue development and repair, and are associated with many diseases (e.g. Pulmonary artery hypertension, Bronchopulmonary dysplasia, ischemic cardiomyopathy, retinopathy and tumor growth). The long-term goal of Dr. Pang’s lab is to identify the essential targets that regulate angiogenesis and vascular remodeling under physiological and pathological conditions. In last 15 years, her group revealed several novel mechanisms on angiogenesis and vascular remodeling during organ development and vascular diseases, such as GIT1 mediated GPCR signaling and Dll4-Notch signaling. Her group recently developed a novel pipeline, called “Vessel Tech” , for analyzing vascular characteristics using machine learning methods, which provides a powerful tool for vascular biologists. Dr. Pang’s contributions in cardiovascular research fields have been evidenced by being the winner of the AHA Cournand and Comroe Young Investigator Award, AHA SDG award and AHA IPA awards and total 48 publications including Circulation, Cell Report, Hypertension et al. She has served as a reviewer of the cardiovascular-related journals, as well as the reviewer of NHLBI, Department of Defense and AHA.
Abstract: Clinical trials of Dll4 (Delta-like 4) neutralizing antibodies (Dll4nAbs) in cancer patients are ongoing. Surprisingly, pulmonary hypertension (PH) occurs in 14% to 18% of patients treated with Dll4nAbs, but the mechanisms have not been studied. Here, PH progression was measured in mice treated with Dll4nAbs. We detected Notch signaling in lung tissues and analyzed pulmonary vascular permeability and inflammation. Notch target gene array was performed on adult human pulmonary microvascular endothelial cells (ECs) after inhibiting Notch cleavage. Similar mechanisms were studied in PH mouse models and pulmonary arterial hypertension patients. The rescue effects of constitutively activated Notch1 in vivo were also measured. We observed that Dll4nAbs induced PH in mice as indicated by significantly increased right ventricular systolic pressure, as well as pulmonary vascular and right ventricular remodeling. Mechanistically, Dll4nAbs inhibited Notch1 cleavage and subsequently impaired lung endothelial barrier function and increased immune cell infiltration in vessel walls. In vitro, Notch targeted genes' expression related to cell growth and inflammation was decreased in human pulmonary microvascular ECs after the Notch1 inactivation. In lungs of PH mouse models and pulmonary arterial hypertension patients, Notch1 cleavage was inhibited. Consistently, EC cell-cell junction was leaky, and immune cell infiltration increased in PH mouse models. Overexpression activated Notch1-attenuated progression of PH in mice. In conclusion, Dll4nAbs led to PH development in mice by impaired EC barrier function and increased immune cell infiltration through inhibition of Notch1 cleavage in lung ECs. Reduced Notch1 cleavage in lung ECs could be an underlying mechanism of PH pathogenesis.
Ke Yuan
Ke Yuan
Ke Yuan
Ke Yuan
Ke Yuan
Xiaobo Zhou
Harvard Medical School, Boston Children’s Hospital
Meeting ID: 882 6560 8874
Passcode: 898156
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Xiaobo Zhou, Ph.D.
Director of Functional Genomics Laboratory
Brigham and Women's Hospital, Harvard Medical School
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Ke Yuan
CALA Happy Friday Seminar
Feb 18th, 2022
Time: EST 10:30 am; PST: 7:30 am; Beijing time: 11:30pm
Zoom: 849 9682 9273 (Password: 654321)
Engineered ACE2 Decoy Mitigates Lung Injury and Death Induced
by SARS-CoV-2 Variants
Lianghui Zhang, MD & PhD
Assistant Professor
Department of Pharmacology, University of Illinois at Chicago
Bio: Dr. Zhang received her M.D. from Medical School of Fudan University and Ph.D. in Pharmacology from University of Rochester. Dr. Zhang’s research interests have been focused on exploring the mechanisms of inflammatory endothelial injury and repair using acute lung injury mouse model and developing novel mechanism-based regenerative strategies. Her scientific training began with her graduate work under the instruction of Dr. Alan Smrcka at the University of Rochester to dissect signal pathways of cardiac hypertrophy. Dr. Zhang’s postdoctoral training in lung vascular biology was with Dr. Jalees Rehman and Dr. Asrar Malik in the Department of Pharmacology at the University of Illinois at Chicago. She just started to set up her own laboratory. Dr. Zhang is supported by NIH RO1. She has published in high impact journals such as, Nature Chemical Biology, Nature Communications, Circulation, Cell, etc.
Abstract: Vaccine hesitancy and emergence of SARS-CoV-2 variants of concern escaping vaccine-induced immune responses highlight the urgency for novel COVID-19 therapeutics. Engineered ACE2 proteins with augmented binding affinities for SARS-CoV-2 Spike (S) protein may prove to be especially efficacious against multiple variants. Using molecular dynamics simulations, we show that three amino acid substitutions in an engineered soluble ACE2 protein markedly augmented the affinity for the S protein of the SARS-CoV-2 WA-1/2020 isolate as well as multiple variants of concern: B.1.1.7 (Alpha), B.1.351 (Beta), P.1 (Gamma), and B.1.617.2 (Delta). In humanized K18-hACE2 mice infected with SARS-CoV-2 WA-1/2020 or P.1 variant, prophylactic and therapeutic injections of sACE22.v2.4-IgG1 prevented lung vascular injury and edema formation, essential features of CoV-2 induced SARS, and above all improved survival. These studies demonstrate broad efficacy in vivo of an engineered ACE2 decoy against SARS-CoV-2 variants and point to its therapeutic potential.
To view this discussion on the web visit https://groups.google.com/d/msgid/lunginterestgroup/CANnhJiy7EACnkW30vPoPKv14Dmh9tE-_T1eGGBfidUDDMER%3DTg%40mail.gmail.com.
Ke Yuan
Feb 18th, 2022
Time: EST 10:30 am; PST: 7:30 am; Beijing time: 11:30pm
Zoom: 849 9682 9273 (Password: 654321)
Engineered ACE2 Decoy Mitigates Lung Injury and Death Induced
by SARS-CoV-2 Variants
Lianghui Zhang, MD & PhD
Assistant Professor
Department of Pharmacology, University of Illinois at Chicago
Bio: Dr. Zhang received her M.D. from Medical School of Fudan University and Ph.D. in Pharmacology from University of Rochester. Dr. Zhang’s research interests have been focused on exploring the mechanisms of inflammatory endothelial injury and repair using acute lung injury mouse model and developing novel mechanism-based regenerative strategies. Her scientific training began with her graduate work under the instruction of Dr. Alan Smrcka at the University of Rochester to dissect signal pathways of cardiac hypertrophy. Dr. Zhang’s postdoctoral training in lung vascular biology was with Dr. Jalees Rehman and Dr. Asrar Malik in the Department of Pharmacology at the University of Illinois at Chicago. She just started to set up her own laboratory. Dr. Zhang is supported by NIH RO1. She has published in high impact journals such as, Nature Chemical Biology, Nature Communications, Circulation, Cell, etc.
Abstract: Vaccine hesitancy and emergence of SARS-CoV-2 variants of concern escaping vaccine-induced immune responses highlight the urgency for novel COVID-19 therapeutics. Engineered ACE2 proteins with augmented binding affinities for SARS-CoV-2 Spike (S) protein may prove to be especially efficacious against multiple variants. Using molecular dynamics simulations, we show that three amino acid substitutions in an engineered soluble ACE2 protein markedly augmented the affinity for the S protein of the SARS-CoV-2 WA-1/2020 isolate as well as multiple variants of concern: B.1.1.7 (Alpha), B.1.351 (Beta), P.1 (Gamma), and B.1.617.2 (Delta). In humanized K18-hACE2 mice infected with SARS-CoV-2 WA-1/2020 or P.1 variant, prophylactic and therapeutic injections of sACE22.v2.4-IgG1 prevented lung vascular injury and edema formation, essential features of CoV-2 induced SARS, and above all improved survival. These studies demonstrate broad efficacy in vivo of an engineered ACE2 decoy against SARS-CoV-2 variants and point to its therapeutic potential.
Ke Yuan
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Xiaobo Zhou, Ph.D.Associate Professor, Harvard Medical SchoolPhone: 617-525-7866
Director of Functional Genomics Laboratory
Brigham and Women's Hospital, Harvard Medical School
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Ke Yuan
Ke Yuan
CALA Happy Friday Seminar
March 4th, 2022
Time: EST 10:30 am; PST: 7:30 am; Beijing time: 11:30pm
Zoom: 849 9682 9273 (Password: 654321)
A Brief Introduction on Nanopore Sequencing
Hongxu Ding, PhD
Assistant Professor
College of Pharmacy, University of Arizona
Bio: Dr. Ding finished his undergraduate at Tsinghua University in 2013, where he was initially trained as a physicist and later switched to the field of life sciences. He finished his PhD at Columbia University under the instruction of Dr. Andrea Califano in 2018, where he worked on single-cell systems biology. After that, he joined UCSC Genomics Institute as a postdoctoral scholar. Under the supervision of Dr. Joshua Stuart and Dr. Benedict Paten, he continued his work on single-cell analysis, as well as expanded his research to the field of nanopore sequencing. Dr. Ding joined the University of Arizona, College of Pharmacy in 2021 as an assistant professor. The Ding lab (http://dinghongxulab.org/) develops computational biology approaches to interpret single-cell omics profiles and nanopore sequencing readouts.
Abstract: Nanopore sequencing has several prominent advantages, which promise to revolutionize life science research. Specifically, nanopore sequencing is able to 1) generate ultra-long sequencing reads, which greatly facilitate, e.g. de novo genome assembly, genome structural variation detection and RNA splicing isoform detection; 2) profile native DNA/RNA molecules, which opens up possibilities for routinely detecting nucleotide modifications; 3) perform real-time sequencing, which could be used for, e.g. field sequencing and diagnostics.
In my presentation, I will first introduce how does nanopore sequencing work. I will then describe the above-mentioned prominent advantages of nanopore sequencing with basic and clinical research examples. At the end of the presentation, I will report my recent work on nanopore sequencing-based de novo nucleotide modification analysis.
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---------------------------------------------------------------
Xiaobo Zhou, Ph.D.Associate Professor, Harvard Medical SchoolPhone: 617-525-7866
Director of Functional Genomics Laboratory
Brigham and Women's Hospital, Harvard Medical School
The information in this e-mail is intended only for the person to whom it is
addressed. If you believe this e-mail was sent to you in error and the e-mail
contains patient information, please contact the Partners Compliance HelpLine at
http://www.partners.org/complianceline . If the e-mail was sent to you in error
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Ke Yuan
CALA Happy Friday Seminar
March 4th, 2022
Time: EST 10:30 am; PST: 7:30 am; Beijing time: 11:30pm
Zoom: 849 9682 9273 (Password: 654321)
A Brief Introduction on Nanopore Sequencing
Hongxu Ding, PhD
Assistant Professor
College of Pharmacy, University of Arizona
To unsubscribe from this group and stop receiving emails from it, send an email to lunginterestgroup+unsubscribe@googlegroups.com.
To view this discussion on the web visit https://groups.google.com/d/msgid/lunginterestgroup/CAO%2BFyMxRvDTXtdXHHUZALV8P80rRqVWgS4CQuKGhxaxJTd595g%40mail.gmail.com.
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---------------------------------------------------------------
Xiaobo Zhou, Ph.D.Associate Professor, Harvard Medical SchoolPhone: 617-525-7866
Director of Functional Genomics Laboratory
Brigham and Women's Hospital, Harvard Medical School
The information in this e-mail is intended only for the person to whom it is
addressed. If you believe this e-mail was sent to you in error and the e-mail
contains patient information, please contact the Partners Compliance HelpLine at
http://www.partners.org/complianceline . If the e-mail was sent to you in error
but does not contain patient information, please contact the sender and properly
dispose of the e-mail. --
You received this message because you are subscribed to the Google Groups "LungInterestGroup" group.
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Ke Yuan
CALA Happy Friday Seminar
March 4th, 2022
Time: EST 10:30 am; PST: 7:30 am; Beijing time: 11:30pm
Zoom: 849 9682 9273 (Password: 654321)
A Brief Introduction on Nanopore Sequencing
Hongxu Ding, PhD
Assistant Professor
College of Pharmacy, University of Arizona
Bio: Dr. Ding finished his undergraduate at Tsinghua University in 2013, where he was initially trained as a physicist and later switched to the field of life sciences. He finished his PhD at Columbia University under the instruction of Dr. Andrea Califano in 2018, where he worked on single-cell systems biology. After that, he joined UCSC Genomics Institute as a postdoctoral scholar. Under the supervision of Dr. Joshua Stuart and Dr. Benedict Paten, he continued his work on single-cell analysis, as well as expanded his research to the field of nanopore sequencing. Dr. Ding joined the University of Arizona, College of Pharmacy in 2021 as an assistant professor. The Ding lab (http://dinghongxulab.org/) develops computational biology approaches to interpret single-cell omics profiles and nanopore sequencing readouts.
Abstract: Nanopore sequencing has several prominent advantages, which promise to revolutionize life science research. Specifically, nanopore sequencing is able to 1) generate ultra-long sequencing reads, which greatly facilitate, e.g. de novo genome assembly, genome structural variation detection and RNA splicing isoform detection; 2) profile native DNA/RNA molecules, which opens up possibilities for routinely detecting nucleotide modifications; 3) perform real-time sequencing, which could be used for, e.g. field sequencing and diagnostics.
In my presentation, I will first introduce how does nanopore sequencing work. I will then describe the above-mentioned prominent advantages of nanopore sequencing with basic and clinical research examples. At the end of the presentation, I will report my recent work on nanopore sequencing-based de novo nucleotide modification analysis.
Ke Yuan
CALA Happy Friday Seminar
March 4th, 2022
Time: EST 10:30 am; PST: 7:30 am; Beijing time: 11:30pm
Zoom: 849 9682 9273 (Password: 654321)
A Brief Introduction on Nanopore Sequencing
Hongxu Ding, PhD
Assistant Professor
College of Pharmacy, University of Arizona
To unsubscribe from this group and stop receiving emails from it, send an email to lunginterestgroup+unsubscribe@googlegroups.com.
To view this discussion on the web visit https://groups.google.com/d/msgid/lunginterestgroup/CAO%2BFyMxRvDTXtdXHHUZALV8P80rRqVWgS4CQuKGhxaxJTd595g%40mail.gmail.com.
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---------------------------------------------------------------
Xiaobo Zhou, Ph.D.Associate Professor, Harvard Medical SchoolPhone: 617-525-7866
Director of Functional Genomics Laboratory
Brigham and Women's Hospital, Harvard Medical School
The information in this e-mail is intended only for the person to whom it is
addressed. If you believe this e-mail was sent to you in error and the e-mail
contains patient information, please contact the Partners Compliance HelpLine at
http://www.partners.org/complianceline . If the e-mail was sent to you in error
but does not contain patient information, please contact the sender and properly
dispose of the e-mail. --
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Ke Yuan
Ke Yuan
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To view this discussion on the web visit https://groups.google.com/d/msgid/lunginterestgroup/CAO%2BFyMxRvDTXtdXHHUZALV8P80rRqVWgS4CQuKGhxaxJTd595g%40mail.gmail.com.
--
---------------------------------------------------------------
Xiaobo Zhou, Ph.D.Associate Professor, Harvard Medical SchoolPhone: 617-525-7866
Director of Functional Genomics Laboratory
Brigham and Women's Hospital, Harvard Medical School
The information in this e-mail is intended only for the person to whom it is
addressed. If you believe this e-mail was sent to you in error and the e-mail
contains patient information, please contact the Partners Compliance HelpLine at
http://www.partners.org/complianceline . If the e-mail was sent to you in error
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Ke Yuan
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--
---------------------------------------------------------------
Xiaobo Zhou, Ph.D.Associate Professor, Harvard Medical SchoolPhone: 617-525-7866
Director of Functional Genomics Laboratory
Brigham and Women's Hospital, Harvard Medical School
The information in this e-mail is intended only for the person to whom it is
addressed. If you believe this e-mail was sent to you in error and the e-mail
contains patient information, please contact the Partners Compliance HelpLine at
http://www.partners.org/complianceline . If the e-mail was sent to you in error
but does not contain patient information, please contact the sender and properly
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Ke Yuan
Ke Yuan
Ke Yuan
Ke Yuan
Ke Yuan
Dear CALA members,
To unsubscribe from this group and stop receiving emails from it, send an email to lunginterestgr...@googlegroups.com.
To view this discussion on the web visit https://groups.google.com/d/msgid/lunginterestgroup/CAO%2BFyMxRvDTXtdXHHUZALV8P80rRqVWgS4CQuKGhxaxJTd595g%40mail.gmail.com.
--
---------------------------------------------------------------
Xiaobo Zhou, Ph.D.Associate Professor, Harvard Medical SchoolPhone: 617-525-7866
Director of Functional Genomics Laboratory
Brigham and Women's Hospital, Harvard Medical School
The information in this e-mail is intended only for the person to whom it is
addressed. If you believe this e-mail was sent to you in error and the e-mail
contains patient information, please contact the Partners Compliance HelpLine at
http://www.partners.org/complianceline . If the e-mail was sent to you in error
but does not contain patient information, please contact the sender and properly
dispose of the e-mail. --
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Ke Yuan
CALA Happy Friday Seminar
April 15th, 2022
Time: EST 10:30 am; PST: 7:30 am; Beijing time: 10:30pm
Zoom: 849 9682 9273 (Password: 654321)
Leveraging Clues from Stem cells to treat pulmonary arterial hypertension
Jun Yang, PhD
Professor
Department of Physiology, Zhejiang University School of Medicine
Bio: Dr. Jun Yang received her Ph.D. degree from Peking Union Medical College. She carried out post-doctoral studies with Professor Nick Morrell on pulmonary vascular disease at University of Cambridge in 2005 after the training on TGF beta signaling in the USA. She was awarded British Associate of Lung Research and Pfizer European pulmonary vascular disease research young investigator first prize. In 2014, she established an independent group to deploy the stem cell based pulmonary arterial hypertension (PAH) model system to study the role of BMPRII signaling pathway in pulmonary vascular disease. Her group applied stem cell technology on drug screening for small molecular intervention of pulmonary arterial hypertension. She has published more than 30 research papers as first or correspondent author in reputable journal, including European Respiratory Journal, Circulation Research, etc. She is also a young leader of National Key Research and Development Program -Stem Cell project.
Abstract: Recently by using CRISPR/Cas9 and Single-cell RNA sequencing techniques, she has shown that; (a). BMPR2 mutation regulates right ventricular function via inhibition of DNA (ID) genes in congenital heart disease (CHD)-PAH. (b). Identified a compound BUR1 with a new chemical structure by targeting deficient BMPR2 signaling to improve pulmonary vascular remodeling.
Dear CALA members,
To unsubscribe from this group and stop receiving emails from it, send an email to lunginterestgroup+unsubscribe@googlegroups.com.
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---------------------------------------------------------------
Xiaobo Zhou, Ph.D.Associate Professor, Harvard Medical SchoolPhone: 617-525-7866
Director of Functional Genomics Laboratory
Brigham and Women's Hospital, Harvard Medical School
The information in this e-mail is intended only for the person to whom it is
addressed. If you believe this e-mail was sent to you in error and the e-mail
contains patient information, please contact the Partners Compliance HelpLine at
http://www.partners.org/complianceline . If the e-mail was sent to you in error
but does not contain patient information, please contact the sender and properly
dispose of the e-mail. --
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Ke Yuan
Ke Yuan
Ke Yuan
Ke Yuan
Ke Yuan
Ke Yuan
CALA Happy Friday Seminar
May 6th, 2022
Time: EST 10:30 am; PST: 7:30 am; Beijing time: 10:30pm
Zoom: 849 9682 9273 (Password: 654321)
Towards Understanding the Epigenetic Regulation Of Childhood Asthma
Hong Ji, PhD
Assistant Professor
Department of Anatomy, Physiology and Cell biology
School of Veterinary Medicine, University of California, Davis
Ke Yuan
CALA Happy Friday Seminar
May 6th, 2022
Time: EST 10:30 am; PST: 7:30 am; Beijing time: 10:30pm
Zoom: 849 9682 9273 (Password: 654321)
Towards Understanding the Epigenetic Regulation Of Childhood Asthma
Hong Ji, PhD
Assistant Professor
Department of Anatomy, Physiology and Cell biology
School of Veterinary Medicine, University of California, Davis
Bio: Dr. Ji finished her undergraduate at University of Science and Technology of China and obtained her PhD in biological sciences at Vanderbilt University studying telomeres and telomerase. She then moved to Dr. Andy Feinberg's lab at Johns Hopkins School of Medicine and did her postdoctoral training in epigenetics, molecular immunology and cancer. After this, Dr. Ji joined the research faculty at the Cincinnati Children's Hospital Medical Center and started her independent research program in asthma and environmental epigenetics. Her lab is interested in understanding the epigenetic regulation of chronic diseases such as childhood asthma and examining how epigenetic mechanisms mediate the impact of environmental exposures during critical developmental windows (e.g., infancy) on increased disease susceptibility. An integrative approach combining molecular and bioinformatic analysis of methylome, chromatin, gene expression and gene networks with immunologic and physiologic characterization of disease models is utilized to understand disease etiology and progression. Research is performed in animal models, cell culture, and human biologic specimens. In 2018, Dr. Ji joined University of California Davis as a tenure track faculty and as a member of the California National Primate Research Center, expanding her research into the non-human primate model.
Abstract: Dr. Ji's presentation at the CALA seminar series will primarily focus on the role of Tet1 protein, an epigenetic modulator, in regulating asthma pathogenesis. Initially identified from epigenome-wide association studies as a candidate gene for asthma, the role of Tet1 in asthma has been first established by Dr. Ji’s group using a mouse model of allergic airway inflammation. Genes and pathways regulated by Tet1 were discovered and single-cell analysis found that alveolar type II cells and ciliated cells were the main targets of Tet1 in the lung epithelium. Several potential mechanisms through which Tet1 regulates the epigenetic landscape to alter gene expression and protect against lung inflammation will be discussed.
Acknowledgment: We are going to hold an annual CALA meeting in San Francisco on 5/14/2022. Thanks Biocytogen (https://biocytogen.com, Platinum sponsor), Cell Biologics Inc (https://cellbiologics.com, Golden sponsor), and RWD Life Science (https://www.rwdstco.com, Silver sponsor) donation to CALA.
Dear CALA members,
To unsubscribe from this group and stop receiving emails from it, send an email to lunginterestgr...@googlegroups.com.
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--
---------------------------------------------------------------
Xiaobo Zhou, Ph.D.Associate Professor, Harvard Medical SchoolPhone: 617-525-7866
Director of Functional Genomics Laboratory
Brigham and Women's Hospital, Harvard Medical School
The information in this e-mail is intended only for the person to whom it is
addressed. If you believe this e-mail was sent to you in error and the e-mail
contains patient information, please contact the Partners Compliance HelpLine at
http://www.partners.org/complianceline . If the e-mail was sent to you in error
but does not contain patient information, please contact the sender and properly
dispose of the e-mail. --
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Ke Yuan
Dear CALA members,
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To view this discussion on the web visit https://groups.google.com/d/msgid/lunginterestgroup/CAO%2BFyMxRvDTXtdXHHUZALV8P80rRqVWgS4CQuKGhxaxJTd595g%40mail.gmail.com.
--
---------------------------------------------------------------
Xiaobo Zhou, Ph.D.Associate Professor, Harvard Medical SchoolPhone: 617-525-7866
Director of Functional Genomics Laboratory
Brigham and Women's Hospital, Harvard Medical School
The information in this e-mail is intended only for the person to whom it is
addressed. If you believe this e-mail was sent to you in error and the e-mail
contains patient information, please contact the Partners Compliance HelpLine at
http://www.partners.org/complianceline . If the e-mail was sent to you in error
but does not contain patient information, please contact the sender and properly
dispose of the e-mail. --
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Ke Yuan
Ke Yuan
Ke Yuan
Ke Yuan
Ke Yuan
Ke Yuan
CALA Happy Friday Seminar
June 10th, 2022
Time: EST 10:30 am; PST: 7:30 am; Beijing time: 10:30pm
Zoom: 849 9682 9273 (Password: 654321)
Therapeutic targeting Mevalonate-Geranylgeranyl Diphosphate Pathway with Statins Overcomes Chemotherapy-resistance in Small Cell Lung Cancer
Hongbin Ji, PhD
Professor
Shanghai Institute of Biochemistry and Cell Biology
Chinese Academy of Sciences
Bio: Dr. Ji finished his PhD training in biological sciences at Shanghai Institute of Biochemistry, Chinese Academy of Science. He then moved to Harvard Medical School for postdoctoral training. After this, Dr. Ji join the Shanghai Institute of Biochemistry and Cell Biology, Chinese Academy of Sciences. The research interest in Dr. Ji’s lab is to decipher the molecular mechanisms involved in lung cancer initiation, malignant progression, trans-differentiation and metastasis, with a long-term goal to identify effective biomarkers for diagnosis and therapeutic targets for personalized medicine. He has published many high impact papers including Nature Genetics, Nature Cancer, JCI, PNAS, Nature, Cancer Cell.
Abstract: Small cell lung cancer (SCLC) is a recalcitrant cancer that lacks effective treatments to tackle chemotherapy-resistance. Using human SCLC xenografts, we established multiple chemotherapy-resistant mouse models through long-term intermittent chemotherapy, mimicking clinical strategy. We discovered that chemotherapy-resistant SCLC has undergone metabolic reprogramming towards the Mevalonate (MVA)-Geranylgeranyl diphosphate (GGPP) pathway, which can be inhibited by clinically approved statins. Mechanistically, statins reduce chemotherapy-resistant SCLC growth through the GGPS1/RAB7A/autophagy axis via post-translational geranylgeranylation. Statins overcomes both intrinsic and acquired SCLC chemotherapy-resistance in multiple GGPS1 high SCLC PDX models, whereas GGPS1 expression is negatively associated with survival in SCLC patients. Strikingly, combining statins with chemotherapy resulted in durable responses in three patients who relapsed from first-line chemotherapy. Collectively, these data uncover the MVA-GGPP pathway as a metabolic vulnerability in chemotherapy-resistant SCLC and identify statins as a potentially effective treatment to overcome resistance.
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--
---------------------------------------------------------------
Xiaobo Zhou, Ph.D.Associate Professor, Harvard Medical SchoolPhone: 617-525-7866
Director of Functional Genomics Laboratory
Brigham and Women's Hospital, Harvard Medical School
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--
---------------------------------------------------------------
Xiaobo Zhou, Ph.D.Associate Professor, Harvard Medical SchoolPhone: 617-525-7866
Director of Functional Genomics Laboratory
Brigham and Women's Hospital, Harvard Medical School
The information in this e-mail is intended only for the person to whom it is
addressed. If you believe this e-mail was sent to you in error and the e-mail
contains patient information, please contact the Partners Compliance HelpLine at
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Ke Yuan
CALA Happy Friday Seminar
June 24th, 2022
Time: EST 10:30 am; PST: 7:30 am; Beijing time: 10:30pm
Zoom: 849 9682 9273 (Password: 654321)
Electronic Cigarette Exposure Enhances Lung Inflammation, Fibrosis and Metabolic Reprogramming
Xiangming Ji, PhD
Assistant Professor
Georgia State University, Atlanta, GA
Bio: Xiangming Ji, PhD, is an Assistant Professor in the Department of Nutrition. Dr. Ji received his Ph. D from Wayne State University, Detroit, MI, in 2012. After that, he has been working as postdoc fellow at Vanderbilt University Medical Center. Dr. Ji is a molecular biochemist with specialization in lung disease early detection. His research focuses on metabolic studies in the airway epithelium from normal cells to at-risk epithelial cells all the way to cancer cells. The majority of his research is utilize stable isotope tracer to monitor metabolic reprogramming in the airway epithelial compartment at the core of the development of lung diseases such as CF, COPD, and lung cancer. In 2017, Dr. Ji moved to the Georgia State University as an assistant Professor.
Abstract: The goal of the Ji laboratory is to determine the metabolic reprogramming due to the exposure of E-cigarette and traditional cigarette smoking. We employed βENaC-overexpressing mice bearing COPD-like pulmonary abnormality, and exposed them to ENDS. We found that ENDS exposure aggravated airspace enlargement and mucus production in βENaC- overexpressing mice, which was associated with increased MMP12 and Muc5ac, respectively. Plasma from non-smoker controls, cigarette smokers, and END users was collected, and metabolites were identified by UPLC-MS (ultra-performance liquid chromatography mass spectrometer). We found END vaping dysregulated TCA cycle-related metabolites while cigarette smoking altered sphingolipid metabolites.
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--
---------------------------------------------------------------
Xiaobo Zhou, Ph.D.Associate Professor, Harvard Medical SchoolPhone: 617-525-7866
Director of Functional Genomics Laboratory
Brigham and Women's Hospital, Harvard Medical School
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--
---------------------------------------------------------------
Xiaobo Zhou, Ph.D.Associate Professor, Harvard Medical SchoolPhone: 617-525-7866
Director of Functional Genomics Laboratory
Brigham and Women's Hospital, Harvard Medical School
The information in this e-mail is intended only for the person to whom it is
addressed. If you believe this e-mail was sent to you in error and the e-mail
contains patient information, please contact the Partners Compliance HelpLine at
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Ke Yuan
Ke Yuan
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--
---------------------------------------------------------------
Xiaobo Zhou, Ph.D.Associate Professor, Harvard Medical SchoolPhone: 617-525-7866
Director of Functional Genomics Laboratory
Brigham and Women's Hospital, Harvard Medical School
The information in this e-mail is intended only for the person to whom it is
addressed. If you believe this e-mail was sent to you in error and the e-mail
contains patient information, please contact the Partners Compliance HelpLine at
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Ke Yuan
August 12 th , 2022
Time: EST 10:30 am; PST: 7:30 am; Beijing time: 10:30pm
Zoom: 849 9682 9273 (Password: 654321)
Hypertension: A Post-GWAS Approach for Complex Diseases
Wei Sun, MD
Assistant Professor
Division of Cardiology, Heart and Vascular Institute,
University of Pittsburgh Medical Center (UPMC),
Vascular Medicine Institute, University of Pittsburgh
Bio: Dr. Wei Sun obtained his B.M. and M.S. from Beijing Medical University and M.D. from Peking
University Health Science Center. He received his postdoctoral training at the University of California,
Riverside, followed by Internal Medicine residency in Mount Auburn Hospital of Harvard Medical School,
General Cardiology fellowship and NIH T32 fellowship in UPMC. While he practices general cardiology as
an attending physician, he is the principal investigator of functional genomics studies on cardiovascular
diseases including pulmonary hypertension. Dr. Sun is currently the recipient of NIH K08 award, AHA
Career Development Award, and the Jenesis Innovative Research Award for Pulmonary Arterial
Hypertension. His research papers are recently published in Nature Aging, JACC Basic and Translational
Sciences, Circulation, Nature Communications, and Nucleic Acid Research. He is the member of American
Heart Association, Chinese American Heart Association, American College of Cardiology, European Society
of Cardiology, American Medical Association and American College of Physicians.
Abstract: My research interest has focused on the functional genomics analysis of single nucleotide
polymorphisms (SNPs) in complex cardiovascular diseases, including pulmonary arterial hypertension
(PAH). I aim to elucidate the molecular mechanism underlying the emerging genetic features of
complex diseases, utilizing a newly developed platform/pipeline to screen the functionality of single
nucleotide variants that are mostly localized in non-coding regions of the genome and have been
associated with the diseases by Genome-wide Association Studies (GWAS). This post-GWAS analysis
will allow me to identify functional SNPs and the DNA-protein complexes that they bind, to identify novel
pathways in the functional regulation of the disease-associated genetic locus and elucidating a
pathogenic mechanism that combines the acquired environmental triggering factors and altered genetic
susceptibility. This functional genomics approach will be utilized in the discovery, development, and
clinical application of new diagnostic and therapeutic approaches in cardiovascular diseases, including
Ke Yuan
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--
---------------------------------------------------------------
Xiaobo Zhou, Ph.D.Associate Professor, Harvard Medical SchoolPhone: 617-525-7866
Director of Functional Genomics Laboratory
Brigham and Women's Hospital, Harvard Medical School
The information in this e-mail is intended only for the person to whom it is
addressed. If you believe this e-mail was sent to you in error and the e-mail
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Ke Yuan
August 12th, 2022
Time: EST 10:30 am; PST: 7:30 am; Beijing time: 10:30pm
Zoom: 849 9682 9273 (Password: 654321)
The Genetic and Acquired Pathogenesis of Pulmonary Arterial Hypertension: A Post-GWAS Approach for Complex Diseases
Wei Sun, MD
Assistant Professor
Division of Cardiology, Heart and Vascular Institute,
University of Pittsburgh Medical Center (UPMC),
Vascular Medicine Institute, University of Pittsburgh
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--
---------------------------------------------------------------
Xiaobo Zhou, Ph.D.Associate Professor, Harvard Medical SchoolPhone: 617-525-7866
Director of Functional Genomics Laboratory
Brigham and Women's Hospital, Harvard Medical School
The information in this e-mail is intended only for the person to whom it is
addressed. If you believe this e-mail was sent to you in error and the e-mail
contains patient information, please contact the Partners Compliance HelpLine at
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Ke Yuan
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--
---------------------------------------------------------------
Xiaobo Zhou, Ph.D.Associate Professor, Harvard Medical SchoolPhone: 617-525-7866
Director of Functional Genomics Laboratory
Brigham and Women's Hospital, Harvard Medical School
The information in this e-mail is intended only for the person to whom it is
addressed. If you believe this e-mail was sent to you in error and the e-mail
contains patient information, please contact the Partners Compliance HelpLine at
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Ke Yuan
CALA Happy Friday Seminar
August 26th, 2022
Time: EST 10:30 am; PST: 7:30 am; Beijing time: 10:30pm
Zoom: 849 9682 9273 (Password: 654321)
The path to new therapies for pulmonary arterial hypertension:
The story of ACTRIIA-Fc
Peiran Yang, PhD
Assistant Professor
State Key Laboratory of Medical Molecular Biology,
Department of Physiology, Institute of Basic Medical Sciences,
Chinese Academy of Medical Sciences, Peking Union Medical College
Bio: Dr Peiran Yang obtained his BA(Hons) and PhD degrees from the University of Cambridge. During his graduate studies, he was supervised by Professor Anthony Davenport, an expert in receptor pharmacology, and by Professor Nicholas Morrell, an expert in pulmonary vascular disease. His PhD research focused on the apelin receptor and its ligands as potential targets for the treatment of pulmonary arterial hypertension (PAH). With a Parke-Davis fellowship, Dr Yang joined Professor Paul Yu’s group in Brigham and Women’s Hospital, Harvard Medical School, where he conducted research investigating new therapeutic targets and agents for PAH, including Sotatercept. Dr Yang has received the GalaxoSmithKline Award for Young Investigators and the Vogt Prize from the British Pharmacological Society. His research papers are recently published in NEJM, Sci Transl Med and Circulation. Dr Yang has recently joined the Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences as a principal investigator.
Abstract: Dr Yang’s research focuses on respiratory diseases including pulmonary hypertension and fibrosis. He is particularly interested in altered or aberrant cell signaling as a potential disease-causing mechanism and a source of potential drug targets. Human genetics and animal studies implicate loss of function in bone morphogenetic protein (BMP) signaling and maladaptive transforming growth factor–β (TGFβ) signaling as drivers of PAH. Although sharing common receptors and effectors with BMP/TGFβ, the function of activin and growth and differentiation factor (GDF) ligands in PAH are less well defined. ACTRIIA-Fc (equivalent to Sotatercept), a potent GDF8/11 and activin ligand trap, was used to test the roles of these ligands in animal and cellular models of pulmonary hypertension. The pre-clinical efficacy of ACTRIIA-Fc encouraged the clinical trials of Sotatercept on PAH patients, which demonstrated the benefits of the first-in-class anti-remodeling agent.
CALA Happy Friday Seminar
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--
---------------------------------------------------------------
Xiaobo Zhou, Ph.D.Associate Professor, Harvard Medical SchoolPhone: 617-525-7866
Director of Functional Genomics Laboratory
Brigham and Women's Hospital, Harvard Medical School
The information in this e-mail is intended only for the person to whom it is
addressed. If you believe this e-mail was sent to you in error and the e-mail
contains patient information, please contact the Partners Compliance HelpLine at
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--
---------------------------------------------------------------
Xiaobo Zhou, Ph.D.Associate Professor, Harvard Medical SchoolPhone: 617-525-7866
Director of Functional Genomics Laboratory
Brigham and Women's Hospital, Harvard Medical School
The information in this e-mail is intended only for the person to whom it is
addressed. If you believe this e-mail was sent to you in error and the e-mail
contains patient information, please contact the Partners Compliance HelpLine at
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Ke Yuan
Ke Yuan
CALA Happy Friday Seminar
Sept 9th, 2022
Time: EST 10:30 am; PST: 7:30 am; Beijing time: 10:30pm
Zoom: 849 9682 9273 (Password: 654321)
ACE2, an unexpected regulator of immune responses in lung infection and inflammation
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Hongpeng Jia, MDAssistant ProfessorDivision of Pediatric SurgeryJohns Hopkins University School of MedicineBio: Dr. Hongpeng Jia is a faculty member in the Surgery department at Johns Hopkins University School of Medicine. Dr. Jia had medical training in China and got a Master of Science degree in Physiology from Peking Union Medical College of China. He pursued his postdoc training at the University of Montreal in Canada and the University of Iowa in the United States. He became a research faculty in Iowa and then at the University of Pittsburgh. He joined the department of Surgery at Johns Hopkins in 2015 to pursue his career development.Abstract: Dr. Jia’s research has been in the broad field of lung infection and immunity. Since the SARS pandemic in 2003, his research has been focused on the role of Angiotensin-converting enzyme 2 (ACE2) in infectious and inflammatory diseases in the lung. He is one of the few researchers who continued his research interest in ACE2 in the post-SARS era, which makes him a leading figure in ACE2 biology and clinical application research during the COVID pandemic. Dr. Jia has authored and co-authored more than 110 research and review articles. He is a recipient of 3 NIH research awards for investigating the role of ACE2 in viral and bacterial lung infections.
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--
---------------------------------------------------------------
Xiaobo Zhou, Ph.D.Associate Professor, Harvard Medical SchoolPhone: 617-525-7866
Director of Functional Genomics Laboratory
Brigham and Women's Hospital, Harvard Medical School
The information in this e-mail is intended only for the person to whom it is
addressed. If you believe this e-mail was sent to you in error and the e-mail
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Ke Yuan
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Ke Yuan
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CALA Happy Friday Seminar
September 23rd, 2022
Time: EST 10:30 am; PST: 7:30 am; Beijing time: 10:30pm
Zoom: 849 9682 9273 (Password: 654321)
Vacuolar protein sorting 34 Activation Promotes Pulmonary Vascular Smooth Muscle Cell Proliferation in Pulmonary Hypertension
Yuanjun Shen, PhD
Postdoctoral Scholar
Dr. Elena Goncharova lab
Lung Center, Division of Internal Medicine, School of Medicine
University of California, Davis
Bio: Dr. Yuanjun Shen has training in both pharmaceutical and biomedical research. He obtained his Ph.D. from the University of Rhode Island. He then joined Dr. Elena Goncharova’s Laboratory for the postdoctoral training, and started the research on the mechanisms of pulmonary hypertension. He has earned the VMI Postdoctoral Scholar Award (internal research grant from the University of Pittsburgh) and the American Heart Association Postdoctoral Fellowship. During the training, Dr. Shen has been awarded with several travel awards, Jane Morse Award for the best scored abstract in Pulmonary hypertension category (ATS 2022) and the President’s Award (California Thoracic Society Annual Educational Conference 2022) for his presentations. His research has recently been published in Frontiers in Medicine, Circulation Research, Cellular and Molecular Gastroenterology and Hepatology, and Proceedings of the National Academy of Sciences. Dr. Shen is a member of ATS, AHA, PVRI, AAAS and CALA.
Abstract: My research focuses on understanding the mechanisms and development of pulmonary arterial hypertension (PAH). My current project aims to elucidate the status and mechanisms of regulation and function of Class III phosphatidylinositol 3-kinase vacuolar protein sorting 34 (Vps34) in PA vascular cells in PAH. Inhibitory Ser164 phosphorylation of Vps34 (P-Ser164-Vps34) was significantly decreased in smooth muscle alpha-actin (SMA)-positive areas of small remodeled PAs and PA vascular smooth muscle cells (PAVSMC) from PAH patients. Similar to human PAH, we detected a significant decrease of P-Ser164-Vps34 in SMA-positive areas of small remodeled PAs from mice and rats with SU5416/hypoxia-induced PH. Further, treatment of Akt inhibitor VIII or Akt-knockdown in PAH PAVSMC demonstrated that Vps34 activation is Akt-dependent, which is associated with TSC2 deficiency, Vps15 over-accumulation, and increased proliferation and survival. Pharmacological inhibition of Vps34 in PAH PAVSMC by selective inhibitors SAR405 and VPS34-IN1 significantly decreased proliferation and induced apoptosis. Two-week treatment of SAR405 in mice with SU5416/hypoxia-induced PH attenuated pulmonary vascular remodeling. The above results suggest a therapeutic potential of Vps34 inhibition to reduce PAH PAVSMC hyper-proliferation and attenuate pulmonary vascular remodeling in PAH. In conclusion, Akt-dependent Vps34 activation supports proliferation and survival of PAH PAVSMC. Further studies are needed to evaluate the therapeutic potential of Vps34 inhibition against PAH.
CALA Happy Friday Seminar
Ke Yuan
CALA Happy Friday Seminar
September 23rd, 2022
Time: EST 10:30 am; PST: 7:30 am; Beijing time: 10:30pm
Zoom: 849 9682 9273 (Password: 654321)
Vacuolar protein sorting 34 Activation Promotes Pulmonary Vascular Smooth Muscle Cell Proliferation in Pulmonary Hypertension
Yuanjun Shen, PhD
Postdoctoral Scholar
Dr. Elena Goncharova lab
Lung Center, Division of Internal Medicine, School of Medicine
University of California, Davis
Bio: Dr. Yuanjun Shen has training in both pharmaceutical and biomedical research. He obtained his Ph.D. from the University of Rhode Island. He then joined Dr. Elena Goncharova’s Laboratory for the postdoctoral training, and started the research on the mechanisms of pulmonary hypertension. He has earned the VMI Postdoctoral Scholar Award (internal research grant from the University of Pittsburgh) and the American Heart Association Postdoctoral Fellowship. During the training, Dr. Shen has been awarded with several travel awards, Jane Morse Award for the best scored abstract in Pulmonary hypertension category (ATS 2022) and the President’s Award (California Thoracic Society Annual Educational Conference 2022) for his presentations. His research has recently been published in Frontiers in Medicine, Circulation Research, Cellular and Molecular Gastroenterology and Hepatology, and Proceedings of the National Academy of Sciences. Dr. Shen is a member of ATS, AHA, PVRI, AAAS and CALA.
Abstract: My research focuses on understanding the mechanisms and development of pulmonary arterial hypertension (PAH). My current project aims to elucidate the status and mechanisms of regulation and function of Class III phosphatidylinositol 3-kinase vacuolar protein sorting 34 (Vps34) in PA vascular cells in PAH. Inhibitory Ser164 phosphorylation of Vps34 (P-Ser164-Vps34) was significantly decreased in smooth muscle alpha-actin (SMA)-positive areas of small remodeled PAs and PA vascular smooth muscle cells (PAVSMC) from PAH patients. Similar to human PAH, we detected a significant decrease of P-Ser164-Vps34 in SMA-positive areas of small remodeled PAs from mice and rats with SU5416/hypoxia-induced PH. Further, treatment of Akt inhibitor VIII or Akt-knockdown in PAH PAVSMC demonstrated that Vps34 activation is Akt-dependent, which is associated with TSC2 deficiency, Vps15 over-accumulation, and increased proliferation and survival. Pharmacological inhibition of Vps34 in PAH PAVSMC by selective inhibitors SAR405 and VPS34-IN1 significantly decreased proliferation and induced apoptosis. Two-week treatment of SAR405 in mice with SU5416/hypoxia-induced PH attenuated pulmonary vascular remodeling. The above results suggest a therapeutic potential of Vps34 inhibition to reduce PAH PAVSMC hyper-proliferation and attenuate pulmonary vascular remodeling in PAH. In conclusion, Akt-dependent Vps34 activation supports proliferation and survival of PAH PAVSMC. Further studies are needed to evaluate the therapeutic potential of Vps34 inhibition against PAH.
Ke Yuan
Ke Yuan
Ke Yuan
Ke Yuan
CALA Happy Friday Seminar
October 7th, 2022
Time: EST 10:30 am; PST: 7:30 am; Beijing time: 10:30pm
Zoom: 849 9682 9273 (Password: 654321)
Pulmonary Neuroendocrine Cells Sense Succinate to Stimulate Submucosal Gland Contraction
Wenjie Yu, Ph.D
Postdoctoral Associate
Lung Biology & Cystic Fibrosis Research Center,
Carver College of Medicine, the University of Iowa
Howard Hughes Medical Institute
Bio: Dr. Wenjie Yu obtained his B.S. from China Agricultural University and Ph.D. from the University of Iowa. Currently, he is a senior postdoctoral associate in Dr. Michael J. Welsh laboratory of the University of Iowa. His research focuses on the cell biology and physiology of the airway involving in mucus secretion. Using piglets as an animal model, Dr. Yu and colleagues identified cellular and molecular architecture of normal and cystic fibrosis pig airways and submucosal glands. He found that pulmonary neuroendocrine cells, a rare airway surface epithelial cell type, localize in submucosal glands with new chemosensory mechanism and physiological function. His research is recently published in Developmental Cell, PNAS, Am J Respir Cell Mol Biol, and Development.
Abstract: Regulating the function and secretion of submucosal glands is key to respiratory host defense, but when abnormal, submucosal glands contribute to lung disease. We discovered that submucosal glands contain pulmonary neuroendocrine cells (PNECs) that detect succinate, a stress signal that accumulates on the airway surface in response to inflammation and infection. Succinate diffuses down into submucosal glands and activates an apical succinate receptor SUCNR1 on PNECs, increasing the intracellular Ca2+ concentration. PNECs then release ATP, a short-range signal, which stimulates P2Y1 purinergic receptors on myoepithelial cells wrapped tightly around the submucosal glands. As a result, submucosal glands contract. Succinate-triggered gland contraction may complement action of neurotransmitters that induce mucus release but not gland contraction, to promote mucus ejection onto the airway surface. These findings identify a local circuit in which rare PNECs within submucosal glands sense an environmental cue to orchestrate the function of airway glands.
Ke Yuan
Ke Yuan
Ke Yuan
CALA Happy Friday Seminar
October 21st, 2022
Time: EST 10:30 am; PST: 7:30 am; Beijing time: 10:30pm
Zoom: 849 9682 9273 (Password: 654321)
Brainstem Dbh+ Neurons Control Chronic Allergen-Induced Airway Hyperreactivity
Yujuan Su, Ph.D
Postdoctoral Associate
Dr. Xin Sun lab
University of California at San Diego
Bio: Dr. Yujuan Su obtained her B.S. from Shandong University in China and completed Ph.D. training at the Institute of Neuroscience, Chinese Academy of Sciences in China. Currently, she is an assistant project scientist after completing postdoc research in Dr. Xin Sun’s lab at the University of California at San Diego. Yujuan started her postdoc work with systematically whole-tissue mapping of the lung-innervating sensory neurons. This part of work has awarded her the American Heart Association (AHA) fellowship and a first author publication at AJP-lung. The bulk of her study on functional mapping of the allergen circuit is in review now. Yujuan presented this work at the Lung Gordon Research Conference in 2021, and it was enthusiastic received. She has also been selected to give an oral presentation at the Vertebrate Sensory Keystone Conference later this month. Yujuan’s training in neuroscience and lung biology makes her well-suited to continue to study the interoception interface between the lung and the central nervous system.
Abstract: Chronic exposure of the lung to irritants such as allergen is a primary cause of asthma characterized by exaggerated airway constriction, also called hyperreactivity, which can be life-threatening. Aside from immune cells, vagal sensory neurons are important for airway hyperreactivity. However, the identity and signature of the downstream nodes of this adaptive circuit remains poorly understood. Here we show that a single population of Dbh+ neurons in the nucleus of the solitary tract (nTS) of the brainstem, and downstream neurons in the nucleus ambiguous (NA), are both necessary and sufficient for chronic allergen-induced airway hyperreactivity. We found that repeated exposures of mice to inhaled allergen activates nTS neurons in a mast cell-, interleukin 4 (IL-4)- and vagal nerve-dependent manner. Single-nucleus RNA-seq of the nTS at baseline and following allergen challenges reveals that a Dbh+ population is preferentially activated. Ablation or chemogenetic inactivation of Dbh+ nTS neurons blunted, while chemogenetic activation promoted hyperreactivity. Viral tracing indicates that Dbh+ nTS neurons, capable of producing norepinephrine, project to the NA, and NA neurons are necessary and sufficient to relay allergen signals to postganglionic neurons that then directly drive airway constriction. Focusing on transmitters, delivery of norepinephrine antagonists to the NA blunted allergen-induced hyperreactivity. Together, these findings provide molecular, anatomical and functional definitions of key nodes of a canonical allergen response circuit. The knowledge opens the possibility of targeted neural modulation as an approach to control refractory allergen-induced airway constriction.
Ke Yuan
Ke Yuan
CALA is organizing an International Respiratory Medicine (IRM) Conference 2023 during February 11-13, at Wyndham Lake Buena Vista Resort, Orlando, Florida. This conference intends to bring together CALA members to present most recent research in lung biology and disorders.We believe this conference will be a highly rewarding educational and interacting event for all CALA members.
Please register the conference from the following link.
A discount hotel reservation at the event will be sent to you once you finish the registration.
We look forward to seeing you all at Orlando, Florida.
Best,
IRM Conference 2023 Chairs: Yin Chen, Jianwen Que, Ke Yuan, Zhiyu Dai
Ke Yuan
Ke Yuan
We are going to award one Established Investigator Award, one Junior Investigator Award, one Trainee Award during our CALA meeting this year.
Ke Yuan
Ke Yuan
Ke Yuan
CALA Happy Friday Seminar
December 16th, 2022
Time: EST 10:30 am; PST: 7:30 am; Beijing time: 11:30pm
Zoom: 849 9682 9273 (Password: 654321)
The RNA m6A demethylase, FTO, Regulates Vascular Remodeling in the Pathogenesis of Pulmonary Arterial Hypertension
Jingbo Dai, Ph.D.
Research Assistant Professor
Dr. Youyang Zhao lab
Northwestern University
Bio: Dr. Jingbo Dai obtained his B.E. from China Pharmaceutical University and completed Ph.D. training at the School of Life Sciences and Biotechnology, Shanghai Jiao Tong University. Then he joined Dr. Guofei Zhou’ s laboratory at the University of Illinois at Chicago (UIC) as a postdoc fellow. During his two years in UIC, he studied the smooth muscle cell metabolic reprogramming in pulmonary arterial hypertension (PAH). Jingbo joined Dr. Youyang Zhao’s lab in the Department of Pediatrics at Northwestern University Feinberg School of Medicine and the Ann & Robert H. Lurie Children's Hospital of Chicago in 2018. Currently, he is a research assistant professor and his study focused on the role of Fat mass and obesity-associated protein (FTO), as a major m6A eraser, acts as a key regulator of endothelial cell dysfunction and pulmonary vascular remodeling in the pathogenesis of PAH. This part of work was supported by the American Heart Association (AHA) career development award and Jingbo presented this work at the AHA scientific session in 2022.
Abstract: PAH is a devastating disease characterized by obliterative pulmonary vascular remodeling and progressive elevation of pulmonary vascular resistance that leads to right heart failure and premature death. Post-transcriptional regulation of mRNAs such as N6-methyladenosine (m6A) modifications that can affect expression of key PAH-related genes and pulmonary vascular function remain largely unexplored. We hypothesized that FTO, as a major m6A eraser, acts as a key regulator of endothelial cell dysfunction and pulmonary vascular remodeling in the pathogenesis of PAH. Our study found that FTO expression level is markedly elevated in the endothelial cells of idiopathic PAH (IPAH) patients. The Tie2Cre-Fto (CKO) mice which Fto was disrupted in endothelial cells exhibited inhibited PH under hypoxia treatment as evident by reduced RVSP and lower RV/(LV+S) ratio, indicator of right ventricle hypertrophy. Histological and immunofluorescent staining showed that media layer of pulmonary arteries had less cell proliferation and reduced pulmonary vascular remodeling including wall thickness as well as distal pulmonary arterial muscularization in CKO mice compared with WT mice. Moreover, preclinical MCT-rat PAH model showed attenuated PAH phenotype as well as pulmonary vascular remodeling with pharmacological inhibition of FTO. These studies demonstrate that FTO expression markedly elevates in the EC of IPAH patients. Tie2-Cre mediated loss of FTO in EC protects mice from hypoxia-induced PAH. Thus, targeting FTO is a promising therapeutic strategy for effective treatment of PAH and thereby promoting survival.
Ke Yuan
Ke Yuan
Ke Yuan
As the holiday season approaches, we wanted to take a moment to express our appreciation for all of the hard work and dedication that you have shown to the CALA community and the fight against lung diseases. Your efforts have made a real difference in the research community and the real world lives, and we are grateful to be a part of such a dedicated and compassionate organization.
We hope that you are able to take some time to relax and enjoy the holiday season with your loved ones. We am sending my best wishes to you and your families for a happy and healthy holidays.
Sincerely,
Zhiyu Dai, Ke Yuan and Jianwen Que
Ke Yuan
Ke Yuan
CALA Happy Friday Seminar
January 20th, 2023
Time: EST 10:30 am; PST: 7:30 am; Beijing time: 11:30pm
Zoom: 849 9682 9273 (Password: 654321)
Metabolic Mechanisms of Chemical Toxicity in the Lung
Xinxin Ding, Ph.D.
Professor and Head, Department of Pharmacology and Toxicology, College of Pharmacy
University of Arizona
Bio: Dr. Ding obtained his B.S. from Nanjing University and completed Ph.D. training at The University of Michigan, Ann Arbor. Then he joined the State University of New York (SUNY) at Albany in 1994 as Assistant Professor and became Associate professor in 1997 and Professor in 2004. Dr. Ding joined the University of Arizona as the department Head. His lab studies enzyme function, regulation and genetics as applied to translational research for drug safety and efficacy and genetic and environmental risks for chemical toxicity. Dr. Ding has published more than 200 papers and have been awarded numerous grants from NCI and NIEHS.
Abstract: The ability of many environmental chemicals, including constituents of tobacco smoke, to cause cancer may depend on how efficiently they are bioactivated in the body by biotransformation enzymes, such as the cytochrome P450 monooxygenases. For most chemicals that require bioactivation to cause cancer, it is unclear whether this bioactivation process needs to occur in the target tissue for tumorigenesis, which enzymes or metabolic pathways are most important, or whether variations in the bioactivation enzymes can dictate cancer susceptibility. Dr. Ding will describe the efforts of his laboratory to develop novel approaches and genetically engineered mouse models to address these questions, with a focus on acute lung injury and lung carcinogenesis.
Ke Yuan
CALA Happy Friday Seminar
February 17th, 2023
Time: EST 11:00 am; PST: 8:00 am; Beijing time: 2/18, 12:00 am
Zoom: 849 9682 9273 (Password: 654321)
Host-pathogen interactions in Tuberculosis in the Era of Immunometabolism
Lu Huang, Ph.D.
Assistant Professor, Department of Microbiology and Immunology, College of Medicine
University of Arkansas for Medical Sciences
Bio: Dr. Huang obtained his B.S. in Bioinformatics from Zhejiang University and completed Ph.D. in Immunology at Cornell University, Ithaca. He went on and did his post-doc at Cornell studying the interaction between lung macrophages and Mycobacterium tuberculosis (Mtb). In 2020, Dr. Huang joined the Department of Microbiology and Immunology at the University of Arkansas for Medical Sciences (UAMS) in Little Rock, Arkansas as Assistant Professor. The primary research interest of his lab is to understand the ontogeny and immunometabolism of lung macrophages during Mtb infection.
Abstract: Tuberculosis (TB), a disease caused by Mycobacterium tuberculosis infection, remains one of the biggest infectious disease threats and a leading cause of death worldwide. The lack of understanding of the nature of protective immunity against TB hinders the development of an effective vaccine. During the infection, various types of phagocytes infiltrate to the lung and harbor Mtb. Such complex interactions can further determine the outcome of the disease. Intriguingly, during Mtb infection, different phagocytes exhibit distinct permissiveness, which is regulated by their origins, heterogeneity and metabolism. In this seminar, Dr. Huang will describe the recent progress in his lab on understanding and harnessing the ontogeny and metabolism of lung phagocytes during Mtb infection.
Ke Yuan
Ke Yuan
Ke Yuan
Ke Yuan
CALA Happy Friday Seminar
March 3rd, 2023
Time: EST 9:00 pm; PST: 6:00 pm; Beijing time: 3/4, 10:00 am
Zoom: 849 9682 9273 (Password: 654321)
Tissue resident macrophage function and fate in respiratory virus infection
Bibo Zhu, Ph.D.
Professor, College of Veterinary Medicine, Huazhong Agricultural University;
Hubei Hongshan Laboratory
Bio: Dr. Zhu obtained his Ph.D. in College of Veterinary Medicine at Huazhong Agricultural University. He did post-doc training in Dr. Jie Sun Lab at Indiana University, Mayo Clinic and University of Virginia. His research interests lie in the cellular, molecular, and metabolic mechanisms that govern tissue resident macrophage function and self-renewal during respiratory viral infection including SARS-CoV-2. In 2023, Dr. Zhu joined College of Veterinary Medicine, Huazhong Agricultural University as professor. The future work in his lab will focus on the interaction between animal macrophages and pathogens of critical infectious diseases in livestock and poultry, revealing the mechanisms by which macrophages regulate pathogen infection, providing potential therapeutic target and new ideas for the development of vaccines and novel drugs for animal infectious diseases.
Abstract: Despite the development of many vaccines and highly successful vaccination campaigns, respiratory viruses such as influenza virus and SARS-CoV-2 continue to present a significant public health burden. Lung resident macrophage populations are heterogeneous immune sentinel cells including recruited monocytes, interstitial and alveolar macrophages (AMs). These cells are critical for anti-viral innate immunity and tissue recovery following respiratory viral infection. Conversely, macrophage-derived inflammatory mediators also contribute to pulmonary inflammation and injury. Therefore, understanding the cellular and molecular mechanisms regulating macrophage protective versus pathogenic function is urgently needed for developing novel host-targeting therapeutics against severe viral pneumonia including COVID-19. In this seminar, Dr. Zhu will describe the work completed in postdoc training on understanding the mechanisms modulating tissue macrophage fate choices in vivo and dissecting mechanisms by which inhibition of pyruvate metabolism regulates macrophage inflammation in response to influenza and COVID-19.
Ke Yuan
Ke Yuan
请填写下是否参加2023 ATS Washington DC May 19th 和CALA member的聚会，您的信息将帮助我们更好地组织活动，谢谢！https://docs.google.com/forms/d/1IjC1CZGlrWJ0w_6F657Rfji30KlTLwdom2gVMEEXH4Q/prefill
We are going to award one Established Investigator Award, one Junior Investigator Award, one Trainee Award during our CALA meeting this year.
Please nominate yourself, your colleague, trainee for the awards. Please send your nomination to our award committee chair Dr. Jianwen Que, jq2...@cumc.columbia.edu by Friday 3/17. Thanks.
CALA committee
Beiyun Zhou
Hi Ke,
Somehow it shows “Gathering at San Francisco at ATS 2022 meeting”?
Beiyun
From: lunginte...@googlegroups.com <lunginte...@googlegroups.com>
On Behalf Of Ke Yuan
Sent: Thursday, March 2, 2023 3:38 PM
To: lunginte...@googlegroups.com
Subject: Re: CALA 2022 Friday Happy Hour Series
请填写下是否参加2023 ATS Washington DC May 19th 和CALA member的聚会，您的信息将帮助我们更好地组织活动，谢谢！https://docs.google.com/forms/d/1IjC1CZGlrWJ0w_6F657Rfji30KlTLwdom2gVMEEXH4Q/prefill
CALA committee
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Ke Yuan
To view this discussion on the web visit https://groups.google.com/d/msgid/lunginterestgroup/BY5PR07MB6514D8817052E8A7DE1A8036AFB29%40BY5PR07MB6514.namprd07.prod.outlook.com.
Ke Yuan
Ke Yuan
CALA Happy Friday Seminar
March 17th, 2023
Time: EST 9:00 pm; PST: 6:00 pm; Beijing time: 3/18, 10:00 am
Zoom: 849 9682 9273 (Password: 654321)
Lung Resident T Cell Regulation During Influenza Infections
Weishan Huang, Ph.D.
Associate Professor, Louisiana State University
Bio: Dr. Huang received her undergraduate training at Tsinghua University and did her PhD research at the Cornell University. Following her postdoctoral fellowship and research faculty appointment in immunology at Cornell University, Dr. Huang started her independent research on T cell regulation and memory development at the Louisiana State University, with an adjunct appointment at Cornell University. Beyond her primary appointment, Dr. Huang serves as an associate editor for Frontiers in Immunology and Journal of Medical Virology. She is an active reviewer on NIH study sections. Dr. Huang is an advocate of academic diversity and women in STEM. She is a committee member of the AAI Committee on the Status of Women.
Abstract: Influenza infection is one of the leading causes of morbidity and mortality globally. Lung tissue resident T cells are critical in host defense but may also mediate lung tissue injuries, following flu infections. We are particularly interested in the roles of the regulatory and helper functions of lung resident T cells in balancing the effector immunity and immunopathology. TCR signaling is fundamental for lung resident regulatory T cell differentiation, while the T cell master transcription factor TCF1 is indispensable for lung resident helper T cell development. This seminar will summarize recent findings in Huang lab, focusing on the role of TCR signaling and TCF1 master function in lung resident T cell regulation during flu.
2. Please fill in this updated form for CALA 2023 May 20th Dinner at ATS
https://docs.google.com/forms/d/e/1FAIpQLSd5EwJS8KS0Fr7HWKHTez723wXkl8XM9YTR_5MkxoyDAju3FA/viewform
3. We are going to award one Established Investigator Award, one Junior Investigator Award, one Trainee Award during our CALA meeting this year.
Please nominate yourself, your colleague, trainee for the awards. Please send your nomination to our award committee chair Dr. Jianwen Que, jq2...@cumc.columbia.edu by Friday 3/17. Thanks.
CALA committeeKe Yuan
CALA Happy Friday Seminar
March 17th, 2023