Abstract
BackgroundAlthough adipose stromal cells (ASCs) retain the ability to transdifferentiate at low rate towards the cardiac lineage, the potential mechanisms underlying such process have still to be elucidated. MethodsSince chromatin state modifications are involved in several processes regulating the cellular cell fate commitment, we aimed at evaluating the role of histone protein acetylation in the cardiovascular-like transdifferentiation of ASCs. ResultsWe found a clear increase of histone 3 acetylation status paralleled by a significant upregulation of cardiac TnI gene expression, in ASCs treated with the conditioned medium of primary cardiomyocyte cell cultures for 72h. This result suggests that histone acetylation contributes to the transdifferentiation of ASCs towards the cardiac lineage. In order to directly test this hypothesis, ASCs cultured with regular medium were treated with SAHA, a pan histone deacetylase inhibitor. We found that SAHA enhanced the cardiac permissive state of ASCs, increasing both mRNA and protein expression of cardiovascular genes, particularly cTnI. This suggests that histone acetylation induction is sufficient to promote cardiovascular transdifferentiation. ConclusionsThe control of ASC fate by epigenetic regulators might be an interesting tool to boost both cardiac commitment and regenerative capacities of ASCs.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
