Atheros
Vita Wanberg
Phosphatase and tensin analog (PTEN) gene mutation has been proven for pro-inflammatory property and proliferative potential through tyrosine kinase pathway. We studied mutated PTEN for its pathogenetic association in arterial atherosclerosis.
The objective was to study mutation of PTEN by immunohistochemical method in arterial atherosclerotic lesions and correlate with grades of atherosclerosis, smooth muscle migration in intima, degree of inflammation and Framingham heart study risk factors.
We studied patients with arterial occlusive disease diagnosed by Doppler ultrasonography over a 2-year period. Immunohistochemistry was performed with mouse monoclonal antibodies for PTEN and smooth muscle actin (SMA).
Aorta was the single most common vessel affected (21%). Mean age of patients studied was 48.6 years and 80% were male. Mutant PTEN was associated with higher grades of atherosclerotic lesions (P < 0.0001) graded by American Heart Association classification and with smooth muscle proliferation and migration in intima (P < 0.0001). No statistically significant association with the vessel wall inflammation and other risk factors of atherosclerosis.
Soluble proteins in aortic smooth muscle cells cultured from atherosclerosis-susceptible White Carneau and atherosclerosis-resistant Show Racer pigeons were extracted and separated on 2-dimensional electrophoresis gels. Spots were analyzed with Phoretix software and compared between the 2 breeds. Proteins differentially expressed were arrayed on a map, plotting molecular weight against isoelectric point. Eight discrete zones were identified, 5 that included only proteins unique to susceptible cells and 3 that included proteins unique to resistant cells. Of the 88 differentially expressed proteins from susceptible cells, 41 were located in unique zones, whereas 29 of 82 differentially expressed proteins from resistant cells were in unique zones. Selected proteins from susceptibility, and resistance zones were annotated by peptide mass fragments, molecular weights, isoelectric points, and correspondence with genes differentially expressed between cells from the 2 breeds. Some of the annotated proteins (such as smooth muscle myosin phosphatase, myosin heavy chain, fatty acid-binding protein, ribophorin, heat shock protein, and tumor necrosis factor alpha-inducing factor) corresponded to the current hypotheses to explain atherogenesis. In addition, the unique electrophoretic migration zones of proteins associated with susceptibility or resistance should prove useful as a diagnostic tool in clinical settings where species or phenotypes, or both, susceptible or resistant to atherosclerosis can be identified.
Atherosclerosis is an inflammatory process similar to scar formation in the inner wall of the artery. It is the underlying cause of heart attacks and some strokes. Atherosclerotic lesions in the artery wall are called plaques. 3D ultrasound (US) has been used to monitor the progression of carotid vessel plaques in symptomatic and asymptomatic patients. Different ways of measuring various ultrasound phenotypes of atherosclerosis have been developed. Here, we report on the development and application of a method used to analyze changes in carotid plaque morphology from 3D US. In an effort to extend our previous work in plaque thickness analysis, we developed a procedure that facilitates the visualization and comparison of the distribution of plaque thickness by mapping the 3D arterial structure into a 2D plane.
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B. Chiu, M. Egger, J. D. Spence, G. Parraga and A. Fenster, "Quantification of progression and regression of carotid vessel atherosclerosis using 3D ultrasound images," 2006 International Conference of the IEEE Engineering in Medicine and Biology Society, New York, NY, 2006, pp. 3819-3822.
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