ArticleInternational journal of physiology, pathophysiology and pharmacology2010
Sm22α transcription occurs at the early onset of the cardiovascular system and the intron 1 is dispensable for its transcription in smooth muscle cells during mouse development.
Article in International journal of physiology, pathophysiology and pharmacology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 16 citations in OpenAlex.
- Transgelin defines pro-tumorigenic cancer-associated fibroblasts in pancreatic cancer.British journal of cancer · 2026Article
- TGFβ1 Regulates Cellular Composition of In Vitro Cardiac Perivascular Niche Based on Cardiospheres.Bulletin of experimental biology and medicine · 2024Article
- SM22α deficiency: promoting vascular fibrosis via SRF-SMAD3-mediated activation ofResearch square · 2024Article
- Deletion of SM22α disrupts the structure and function of caveolae and T-tubules in cardiomyocytes, contributing to heart failure.PloS one · 2022Article
- Multiple genotype-phenotype association study reveals intronic variant pair on SIDT2 associated with metabolic syndrome in a Korean population.Human genomics · 2018Article
- Insulin-independent GLUT4 translocation in proliferative vascular smooth muscle cells involves SM22α.Journal of molecular medicine (Berlin, Germany) · 2017Article
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- Systematic selection of small molecules to promote differentiation of embryonic stem cells and experimental validation for generating cardiomyocytes.Cell death discovery · 2016Article
- α5 and αv integrins cooperate to regulate vascular smooth muscle and neural crest functions in vivo.Development (Cambridge, England) · 2015Article
- Review
- An essential requirement for β1 integrin in the assembly of extracellular matrix proteins within the vascular wall.Developmental biology · 2012Article
- Article
- Arterial injury promotes medial chondrogenesis in Sm22 knockout mice.Cardiovascular research · 2011Article
- Disruption of SM22 promotes inflammation after artery injury via nuclear factor kappaB activation.Circulation research · 2010Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
SM22α, also known as SM22, has been widely used as a smooth muscle cell (SMC) marker and is known to be expressed in the embryonic heart. The intron 1 of Sm22 contains multiple important and evolutionarily conserved regulatory elements. To determine the role of the intron 1 in Sm22 transcriptional regulation and the function of SM22 during development, we generated a Sm22 knockout mouse by replacing the intron 1 and the translation initiation with a nuclear localized LacZ (nLacZ) reporter. The resulting Sm22 knockout mice (Sm22(-)/(-)) were viable and fertile without any apparent developmental defects. Using X-gal staining assay, we found that Sm22 transcription was detectable in the chorion formation region and in the heart field before formation of the heart tube at E7.5, namely much earlier than the looped heart stage where it had been previously reported. The expression of lacZ progressively expanded throughout the heart tube by E8.5. LacZ was transiently expressed in the heart and somites and then became restricted to the vascular and visceral SMC organs. These results indicate that SM22 is not required for mouse basal homeostatic function and that the intron 1 is dispensable for Sm22 transcription during development. Given the importance of vasculature in organogenesis and in diseases, this mouse line may be a valuable tool to trace the development and pathology of the cardiovascular system.
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Identifiers
20428474PMC2860299W290676631What OpenQuestion holds
Registered trials
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