ArticleStem cells and development2018
P53 Promotes Retinoid Acid-induced Smooth Muscle Cell Differentiation by Targeting Myocardin.
Article in Stem cells and development, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 15 citations in OpenAlex.
- Myeloid Ecotropic Viral Integration Site 1 Promotes Vascular Smooth Muscle Differentiation through Activation of Myocardin.bioRxiv : the preprint server for biology · 2026Article
- Myogenic Anti-Nucleolin Aptamer iSN04 Inhibits Proliferation and Promotes Differentiation of Vascular Smooth Muscle Cells.Biomolecules · 2024Article
- Protective role of chaperone-mediated autophagy against atherosclerosis.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Exosomal LINC00174 derived from vascular endothelial cells attenuates myocardial I/R injury via p53-mediated autophagy and apoptosis.Molecular therapy. Nucleic acids · 2021Article
- MBNL1 regulates isoproterenol-induced myocardial remodelling in vitro and in vivo.Journal of cellular and molecular medicine · 2021Article
- TL1A inhibits atherosclerosis in apoE-deficient mice by regulating the phenotype of vascular smooth muscle cells.The Journal of biological chemistry · 2020Article
- Identification and activity of the functional complex between hnRNPL and the pseudoexfoliation syndrome-associated lncRNA, LOXL1-AS1.Human molecular genetics · 2020Article
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
TP53 is a widely studied tumor suppressor gene that controls various cellular functions, including cell differentiation. However, little is known about its functional roles in smooth muscle cells (SMCs) differentiation from embryonic stem cells (ESCs). SMC differentiation is at the heart of our understanding of vascular development, normal blood pressure homeostasis, and the pathogenesis of vascular diseases such as atherosclerosis, hypertension, restenosis, as well as aneurysm. Using retinoid acid (RA)-induced SMC differentiation models, we observed that p53 expression is increased during in vitro differentiation of mouse ESCs into SMCs. Meanwhile, suppression of p53 by shRNA reduced RA-induced SMC differentiation. Mechanistically, we have identified for the first time that Myocardin, a transcription factor that induces muscle cell differentiation and muscle-specific gene expression, is the direct target of p53 by bioinformatic analysis, luciferase reporter assay, and chromatin immunoprecipitation approaches. Moreover, in vivo SMC-selective p53 transgenic overexpression inhibited injury-induced neointimal formation. Taken together, our data demonstrate that p53 and its target gene, Myocardin, play regulatory roles in SMC differentiation. This study may lead to the identification of novel target molecules that may, in turn, lead to novel drug discoveries for the treatment of vascular diseases.
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