Abstract
MicroRNAs regulate target gene expression post-transcriptionally in a myriad of cell types and play critical roles in diverse physiological and pathological processes, including cardiomyocyte development, differentiation, and regeneration. The recent publication in Stem Cell Research and Therapy by Wagh and colleagues reports a novel regulatory role for miR-363 in cardiomyocyte specification. By employing microRNA expression profiling and functional knockdown studies on human embryonic stem cell-derived cardiomyocytes, the authors identified miR-363 as an upstream negative regulator of left ventricular specification transcription factor HAND1.
Highlights
MicroRNAs regulate target gene expression post-transcriptionally in a myriad of cell types and play critical roles in diverse physiological and pathological processes, including cardiomyocyte development, differentiation, and regeneration
* Correspondence: manoj.gupta@joslin.harvard.edu 1Section of Islet Cell and Regenerative Biology, Joslin Diabetes Center, Harvard Medical School, Boston, MA 01125, USA Full list of author information is available at the end of the article cardiac cell renewal in humans [3], indicating the limited proliferation capacity of adult CMs
Some miRNAs have been demonstrated to suppress CM proliferation, including miR-1, miR-133, and the miR-15 family, while other miRNAs have been shown to promote in vivo CM proliferation in rat and mouse models [6,7]. miRNAs could be the best targets for understanding cardiac specialization during differentiation of human embryonic stem cells
Summary
MicroRNAs regulate target gene expression post-transcriptionally in a myriad of cell types and play critical roles in diverse physiological and pathological processes, including cardiomyocyte development, differentiation, and regeneration. This commentary discusses the findings from Wagh and colleagues published in this issue of Stem Cell Research and Therapy demonstrating a critical role for miR-363 in post-transcriptional regulation of CM differentiation via the hand and neural crest derivative expressed HAND1 transcription factor [1].
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