ArticleCardiovascular research2011
Arterial injury promotes medial chondrogenesis in Sm22 knockout mice.
Article in Cardiovascular research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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26 citing papers in PubMed, 40 citations in OpenAlex.
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- Insights into elastic fiber fragmentation: Mechanisms and treatment of aortic aneurysm in Marfan syndrome.Vascular pharmacology · 2023Review
- PAC1 deficiency reduces chondrogenesis in atherosclerotic lesions of hypercholesterolemic ApoE-deficient mice.BMC cardiovascular disorders · 2023Article
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- The Cell Origin and Role of Osteoclastogenesis and Osteoblastogenesis in Vascular Calcification.Frontiers in cardiovascular medicine · 2021Review
- Aggrecan in Cardiovascular Development and Disease.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2020Review
- Superficial and deep zone articular chondrocytes exhibit differences in actin polymerization status and actin-associated moleculesOsteoarthritis and cartilage open · 2020Article
- Salvianolic acid A targeting the transgelin-actin complex to enhance vasoconstriction.EBioMedicine · 2018Article
- PI3Kγ promotes vascular smooth muscle cell phenotypic modulation and transplant arteriosclerosis via a SOX9-dependent mechanism.EBioMedicine · 2018Article
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- Inflammation: a culprit for vascular calcification in atherosclerosis and diabetes.Cellular and molecular life sciences : CMLS · 2015Review
- SMAD3 deficiency promotes vessel wall remodeling, collagen fiber reorganization and leukocyte infiltration in an inflammatory abdominal aortic aneurysm mouse model.Scientific reports · 2015Article
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8 authors at 2 institutions in 1 country.
Funding
Abstract
aimsExpression of SM22 (also known as SM22alpha and transgelin), a vascular smooth muscle cells (VSMCs) marker, is down-regulated in arterial diseases involving medial osteochondrogenesis. We investigated the effect of SM22 deficiency in a mouse artery injury model to determine the role of SM22 in arterial chondrogenesis. METHODS AND
resultsSm22 knockout (Sm22(-/-)) mice developed prominent medial chondrogenesis 2 weeks after carotid denudation as evidenced by the enhanced expression of chondrogenic markers including type II collagen, aggrecan, osteopontin, bone morphogenetic protein 2, and SRY-box containing gene 9 (SOX9). This was concomitant with suppression of VSMC key transcription factor myocardin and of VSMC markers such as SM α-actin and myosin heavy chain. The conversion tendency from myogenesis to chondrogenesis was also observed in primary Sm22(-/-) VSMCs and in a VSMC line after Sm22 knockdown: SM22 deficiency altered VSMC morphology with compromised stress fibre formation and increased actin dynamics. Meanwhile, the expression level of Sox9 mRNA was up-regulated while the mRNA levels of myocardin and VSMC markers were down-regulated, indicating a pro-chondrogenic transcriptional switch in SM22-deficient VSMCs. Furthermore, the increased expression of SOX9 was mediated by enhanced reactive oxygen species production and nuclear factor-κB pathway activation.
conclusionThese findings suggest that disruption of SM22 alters the actin cytoskeleton and promotes chondrogenic conversion of VSMCs.
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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.