ArticleExperimental and molecular pathology2010
Disruption of actin cytoskeleton mediates loss of tensile stress induced early phenotypic modulation of vascular smooth muscle cells in organ culture.
Article in Experimental and molecular pathology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 21 citations in OpenAlex.
- Small nucleolar RNA host gene 18 controls vascular smooth muscle cell contractile phenotype and neointimal hyperplasia.Cardiovascular research · 2024Article
- SM22α deficiency: promoting vascular fibrosis via SRF-SMAD3-mediated activation ofResearch square · 2024Article
- Long noncoding RNAProceedings of the National Academy of Sciences of the United States of America · 2018Article
- An overview of potential molecular mechanisms involved in VSMC phenotypic modulation.Histochemistry and cell biology · 2016Review
- Article
- MicroRNA-15b/16 Attenuates Vascular Neointima Formation by Promoting the Contractile Phenotype of Vascular Smooth Muscle Through Targeting YAP.Arteriosclerosis, thrombosis, and vascular biology · 2015Article
- Mechanisms underlying a decrease in KCl-induced contraction after long-term serum-free organ culture of rat isolated mesenteric artery.The Journal of veterinary medical science · 2014Article
- Molecular mechanisms of thoracic aortic dissection.The Journal of surgical research · 2013Review
- Transforming growth factor-β1-induced transcript 1 protein, a novel marker for smooth muscle contractile phenotype, is regulated by serum response factor/myocardin protein.The Journal of biological chemistry · 2011Article
- Arterial injury promotes medial chondrogenesis in Sm22 knockout mice.Cardiovascular research · 2011Article
- Resveratrol induces p53 and suppresses myocardin-mediated vascular smooth muscle cell differentiation.Toxicology letters · 2010Article
- Disruption of SM22 promotes inflammation after artery injury via nuclear factor kappaB activation.Circulation research · 2010Article
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Authors and funding
5 authors at 2 institutions in 1 country.
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Abstract
Aorta organ culture has been widely used as an ex vivo model for studying vessel pathophysiology. Recent studies show that the vascular smooth muscle cells (VSMCs) in organ culture undergo drastic dedifferentiation within the first few hours (termed early phenotypic modulation). Loss of tensile stress to which aorta is subject in vivo is the cause of this early phenotypic modulation. However, no underlying molecular mechanism has been discovered thus far. The purpose of the present study is to identify intracellular signals involved in the early phenotypic modulation of VSMC in organ culture. We find that the drastic VSMC dedifferentiation is accompanied by accelerated actin cytoskeleton dynamics and downregulation of SRF and myocardin. Among the variety of signal pathways examined, increasing actin polymerization by jasplakinolide is the only one hindering VSMC dedifferentiation in organ culture. Moreover, jasplakinolide reverses actin dynamics during organ culture. Latrunculin B (disrupting actin cytoskeleton) and jasplakinolide respectively suppressed and enhanced the expression of VSMC markers, SRF, myocardin, and CArG-box-mediated SMC promoters in PAC1, a VSMC line. These results identify actin cytoskeleton degradation as a major intracellular signal for loss of tensile stress-induced early phenotypic modulation of VSMC in organ culture. This study suggests that disrupting actin cytoskeleton integrity may contribute to the pathogenesis of vascular diseases.
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