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A further study has reported that the epigenetic cardiac signature in ADSCMs is based on a combination of low levels of total acetylated histone 3 and high levels of trimethylated lysine 27 [50], whereas a different study has associated the same methylation (H3K27) with the osteogenic differentiation and the acetylation of histones 3 and 4 mainly with the cardiac lineage [46]. This clear discrepancy is likely due to the possibility that MSCs derived from different tissue sources do not share similar epigenetic states [22], thus suggesting a consequent different transdifferentiation potential. By conditioning with PL, we also observed a general acetylation of histone 3 peaking at 48 hours preceded by dimethylation of lysine 9. We might speculate that the shift towards the demethylation, which is associated with a condensed state of histone 3 [46], could represent a preliminary and permissive step to switch on the acetylation. In addition, considering the bivalent activity of the chromatin in MSCs where parallel methylation and acetylation can coexist [50] but also the role of the demethylation of lysine 9 on histone 3 both in adipogenic, chondrogenic, and osteogenic transdifferentiation [46, 51, 52] and in the capacity to escape senescence mechanisms [53], we could suggest that PL is able to target a multipotent gene expression potential in ADMSCs, including the cardiac lineage but concurrently preserving a proliferative stem cell pool and the capacity to transdifferentiate into the mesodermal lineage. In other words, the commitment to the cardiovascular and the mesodermal lineage would not be mutually exclusive. Moreover, our data are in line with a further study, showing that the inhibition of histone acetylation interferes with the mesodermal commitment of PL-grown ADMSCs [54], thus confirming that the acetylation of histone 3 can bear a bivalent function in inducing both cardiac and mesodermal commitment. Since stem cell fate is not solely determined by epigenetic modifications, the functional consequence of the potential ability of PL to induce either cardiovascular or mesodermal transdifferentiation will eventually depend on the tissue microenvironment surrounding the ADMSCs.
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