ArticleArteriosclerosis, thrombosis, and vascular biology2010
Intronic CArG box regulates cysteine-rich protein 2 expression in the adult but not in developing vasculature.
Article in Arteriosclerosis, thrombosis, and vascular biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 17 citations in OpenAlex.
- Cysteine-rich protein 2 deficiency attenuates angiotensin II-induced abdominal aortic aneurysm formation in mice.Journal of biomedical science · 2022Article
- Article
- Modulation of cysteine-rich protein 2 expression in vascular injury and atherosclerosis.Molecular biology reports · 2014Article
- Cysteine-rich protein 2 alters p130Cas localization and inhibits vascular smooth muscle cell migration.Cardiovascular research · 2013Article
- Myocardin-related transcription factor-A complexes activate type I collagen expression in lung fibroblasts.The Journal of biological chemistry · 2011Article
- down-regulation of Kruppel-like factor-4 (KLF4) by microRNA-143/145 is critical for modulation of vascular smooth muscle cell phenotype by transforming growth factor-beta and bone morphogenetic protein 4.The Journal of biological chemistry · 2011Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
objectiveAn absence of cysteine-rich protein 2 (CRP2) enhances vascular smooth muscle cell (VSMC) migration and increases neointima formation after arterial injury; therefore, CRP2 plays an important role in the response to vascular injury. The goal of the present study was to elucidate the molecular mechanisms that preserve CRP2 expression in the adult vasculature and thus might serve to inhibit the response to injury. METHODS AND
resultsWe generated a series of transgenic mice harboring potential Csrp2 regulatory regions with a lacZ reporter. We determined that the 12-kb first intron was necessary for transgene activity in adult but not in developing vasculature. Within the intron we identified a 6.3-kb region that contains 2 CArG boxes. Serum response factor preferentially bound to CArG2 box in gel mobility shift and chromatin immunoprecipitation assays; additionally, serum response factor coactivator myocardin factors activated CRP2 expression via the CArG2 box. Mutational analysis revealed that CArG2 box was important in directing lacZ expression in VSMC of adult vessels.
conclusionsAlthough CRP2 expression during development is independent of CArG box regulatory sites, CRP2 expression in adult VSMC requires CArG2 element within the first intron. Our results suggest that distinct mechanisms regulate CRP2 expression in VSMC that are controlled by separate embryonic and adult regulatory modules.
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