ArticleAmerican journal of physiology. Heart and circulatory physiology2011
Myocardin is differentially required for the development of smooth muscle cells and cardiomyocytes.
Article in American journal of physiology. Heart and circulatory physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 48 citations in OpenAlex.
- Induction of human cardiomyocyte-like cells from fibroblasts by defined factors.Proceedings of the National Academy of Sciences of the United States of America · 2013Trial
- Genetic Animal Models of Cardiovascular Pathologies.Biomedicines · 2025Review
- Plasticity in airway smooth muscle differentiation during mouse lung development.Developmental cell · 2023Article
- Temporal regulation of notch activation improves arteriovenous fistula maturation.Journal of translational medicine · 2022Article
- QKI is a critical pre-mRNA alternative splicing regulator of cardiac myofibrillogenesis and contractile function.Nature communications · 2021Article
- Discovery and progress of direct cardiac reprogramming.Cellular and molecular life sciences : CMLS · 2017Review
- The Invalidation of HspB1 Gene in Mouse Alters the Ultrastructural Phenotype of Muscles.PloS one · 2016Article
- Myocardin regulates vascular smooth muscle cell inflammatory activation and disease.Arteriosclerosis, thrombosis, and vascular biology · 2015Article
- Myocardin in biology and disease.Journal of biomedical research · 2015Review
- Angiotensin II, from vasoconstrictor to growth factor: a paradigm shift.Circulation research · 2014Article
- Overexpression of myocardin induces partial transdifferentiation of human-induced pluripotent stem cell-derived mesenchymal stem cells into cardiomyocytes.Physiological reports · 2014Article
- Cell division cycle 7 mediates transforming growth factor-β-induced smooth muscle maturation through activation of myocardin gene transcription.The Journal of biological chemistry · 2013Article
- Article
- Activation of MRTF-A-dependent gene expression with a small molecule promotes myofibroblast differentiation and wound healing.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Myocardin: new therapeutic agent in vascular disease?Arteriosclerosis, thrombosis, and vascular biology · 2013Article
- Islet1-expressing cardiac progenitor cells: a comparison across species.Development genes and evolution · 2013Review
- A novel in vitro model system for smooth muscle differentiation from human embryonic stem cell-derived mesenchymal cells.American journal of physiology. Cell physiology · 2013Article
- Derivation and maturation of synthetic and contractile vascular smooth muscle cells from human pluripotent stem cells.Cardiovascular research · 2013Article
- miR-1/133a clusters cooperatively specify the cardiomyogenic lineage by adjustment of myocardin levels during embryonic heart development.PLoS genetics · 2013Article
- The actin-MRTF-SRF gene regulatory axis and myofibroblast differentiation.Journal of cardiovascular translational research · 2012Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Myocardin is a serum response factor (SRF) coactivator exclusively expressed in cardiomyocytes and smooth muscle cells (SMCs). However, there is highly controversial evidence as to whether myocardin is essential for normal differentiation of these cell types, and there are no data showing whether cardiac or SMC subtypes exhibit differential myocardin requirements during development. Results of the present studies showed the virtual absence of myocardin(-/-) visceral SMCs or ventricular myocytes in chimeric myocardin knockout (KO) mice generated by injection of myocardin(-/-) embryonic stem cells (ESCs) into wild-type (WT; i.e., myocardin(+/+) ESC) blastocysts. In contrast, myocardin(-/-) ESCs readily formed vascular SMC, albeit at a reduced frequency compared with WT ESCs. In addition, myocardin(-/-) ESCs competed equally with WT ESCs in forming atrial myocytes. The ultrastructural features of myocardin(-/-) vascular SMCs and cardiomyocytes were unchanged from their WT counterparts as determined using a unique X-ray microprobe transmission electron microscopic method developed by our laboratory. Myocardin(-/-) ESC-derived SMCs also showed normal contractile properties in an in vitro embryoid body SMC differentiation model, other than impaired thromboxane A2 responsiveness. Together, these results provide novel evidence that myocardin is essential for development of visceral SMCs and ventricular myocytes but is dispensable for development of atrial myocytes and vascular SMCs in the setting of chimeric KO mice. In addition, results suggest that as yet undefined defects in development and/or maturation of ventricular cardiomyocytes may have contributed to early embryonic lethality observed in conventional myocardin KO mice and that observed deficiencies in development of vascular SMC may have been secondary to these defects.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.