ArticleArteriosclerosis, thrombosis, and vascular biology2011
Smooth muscle calponin: an unconventional CArG-dependent gene that antagonizes neointimal formation.
Article in Arteriosclerosis, thrombosis, and vascular biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
24 citing papers in PubMed, 34 citations in OpenAlex.
- Comparative transcriptomic analysis of endometrial tissue associated with uterine fibroids and endometrial polyps.Scientific reports · 2026Article
- MAPK14 converges on key transcriptional machinery to promote vascular smooth muscle cell degeneration in abdominal aortic aneurysm.Signal transduction and targeted therapy · 2026Article
- The new perspective on understanding the mechanisms of cardiovascular diseases development.Scientific reports · 2025Article
- Olsenella scatoligenes-derived skatole promotes smooth muscle cell proliferation and migration to aggravate atherosclerosis.The ISME journal · 2025Article
- Disturbed flow regulates protein disulfide isomerase A1 expression via microRNA-204.Frontiers in physiology · 2024Article
- Single-cell transcriptomics uncovers a non-autonomous Tbx1-dependent genetic program controlling cardiac neural crest cell development.Nature communications · 2023Article
- Mediator Med23 deficiency in smooth muscle cells prevents neointima formation after arterial injury.Cell discovery · 2021Article
- Serum response factor-cofactor interactions and their implications in disease.The FEBS journal · 2021Review
- Neuronal regulation of the blood-brain barrier and neurovascular coupling.Nature reviews. Neuroscience · 2020Review
- Coronary Disease-Associated GeneCirculation research · 2020Article
- Vascular smooth muscle-MAPK14 is required for neointimal hyperplasia by suppressing VSMC differentiation and inducing proliferation and inflammation.Redox biology · 2019Article
- CRISPR links to long noncoding RNA function in mice: A practical approach.Vascular pharmacology · 2019Review
- Contribution of p62/SQSTM1 to PDGF-BB-induced myofibroblast-like phenotypic transition in vascular smooth muscle cells lacking Smpd1 gene.Cell death & disease · 2018Article
- Dual Function for Mature Vascular Smooth Muscle Cells During Arteriovenous Fistula Remodeling.Journal of the American Heart Association · 2017Article
- Three-Dimensional Coculture Model to Analyze the Cross Talk Between Endothelial and Smooth Muscle Cells.Tissue engineering. Part C, Methods · 2017Article
- Large-scale identification of human cerebrovascular proteins: Inter-tissue and intracerebral vascular protein diversity.PloS one · 2017Article
- MYOSLID Is a Novel Serum Response Factor-Dependent Long Noncoding RNA That Amplifies the Vascular Smooth Muscle Differentiation Program.Arteriosclerosis, thrombosis, and vascular biology · 2016Article
- Review
- Noncoding RNAs in smooth muscle cell homeostasis: implications in phenotypic switch and vascular disorders.Pflugers Archiv : European journal of physiology · 2016Review
- The short and long of noncoding sequences in the control of vascular cell phenotypes.Cellular and molecular life sciences : CMLS · 2015Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
objectiveSmooth muscle calponin (CNN1) contains multiple conserved intronic CArG elements that bind serum response factor and display enhancer activity in vitro. The objectives here were to evaluate these CArG elements for activity in transgenic mice and determine the effect of human CNN1 on injury-induced vascular remodeling. METHODS AND
resultsMice carrying a lacZ reporter under control of intronic CArG elements in the human CNN1 gene failed to show smooth muscle cell (SMC)-restricted activity. However, deletion of the orthologous sequences in mice abolished endogenous Cnn1 promoter activity, suggesting their necessity for in vivo Cnn1 expression. Mice carrying a 38-kb bacterial artificial chromosome (BAC) harboring the human CNN1 gene displayed SMC- restricted expression of the corresponding CNN1 protein, as measured by immunohistochemistry and Western blotting. Extensive BAC recombineering studies revealed the absolute necessity of a single intronic CArG element for correct SMC-restricted expression of human CNN1. Overexpressing human CNN1 suppressed neointimal formation following arterial injury. Mice with an identical BAC carrying mutations in CArG elements that inhibit human CNN1 expression showed outward remodeling and neointimal formation.
conclusionsA single intronic CArG element is necessary but insufficient for proper CNN1 expression in vivo. CNN1 overexpression antagonizes arterial injury-induced neointimal formation.
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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.