ArticleThe Journal of biological chemistry2015
Expression of V3 Versican by Rat Arterial Smooth Muscle Cells Promotes Differentiated and Anti-inflammatory Phenotypes.
Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 22 citations in OpenAlex.
- The role of splicing events in the inflammatory response of atherosclerosis: molecular mechanisms and modulation.Frontiers in immunology · 2024Review
- V3: an enigmatic isoform of the proteoglycan versican.American journal of physiology. Cell physiology · 2023Review
- The Contribution of Vascular Proteoglycans to Atherothrombosis: Clinical Implications.International journal of molecular sciences · 2023Review
- Deletion of type VIII collagen reduces blood pressure, increases carotid artery functional distensibility and promotes elastin deposition.Matrix biology plus · 2021Article
- Targeting Versican as a Potential Immunotherapeutic Strategy in the Treatment of Cancer.Frontiers in oncology · 2021Review
- The synthesis and secretion of versican isoform V3 by mammalian cells: A role for N-linked glycosylation.Matrix biology : journal of the International Society for Matrix Biology · 2020Article
- Versican-A Critical Extracellular Matrix Regulator of Immunity and Inflammation.Frontiers in immunology · 2020Review
- Dissecting the role of hyaluronan synthases in the tumor microenvironment.The FEBS journal · 2019Review
- A role for proteoglycans in vascular disease.Matrix biology : journal of the International Society for Matrix Biology · 2018Review
- Proteoglycans as Immunomodulators of the Innate Immune Response to Lung Infection.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2018Review
- Provisional matrix: A role for versican and hyaluronan.Matrix biology : journal of the International Society for Matrix Biology · 2017Review
- Vascular Smooth Muscle Cells.Arteriosclerosis, thrombosis, and vascular biology · 2016Review
- G1 Domain of Versican Regulates Hyaluronan Organization and the Phenotype of Cultured Human Dermal Fibroblasts.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2016Article
- Extrinsic and Intrinsic Mechanisms by Which Mesenchymal Stem Cells Suppress the Immune System.The ocular surface · 2016Review
- Postnatal Deletion of the Type II Transforming Growth Factor-β Receptor in Smooth Muscle Cells Causes Severe Aortopathy in Mice.Arteriosclerosis, thrombosis, and vascular biology · 2015Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Arterial smooth muscle cells (ASMCs) undergo phenotypic changes during development and pathological processes in vivo and during cell culture in vitro. Our previous studies demonstrated that retrovirally mediated expression of the versican V3 splice variant (V3) by ASMCs retards cell proliferation and migration in vitro and reduces neointimal thickening and macrophage and lipid accumulation in animal models of vascular injury and atherosclerosis. However, the molecular pathways induced by V3 expression that are responsible for these changes are not yet clear. In this study, we employed a microarray approach to examine how expression of V3 induced changes in gene expression and the molecular pathways in rat ASMCs. We found that forced expression of V3 by ASMCs affected expression of 521 genes by more than 1.5-fold. Gene ontology analysis showed that components of the extracellular matrix were the most significantly affected by V3 expression. In addition, genes regulating the formation of the cytoskeleton, which also serve as markers of contractile smooth muscle cells (SMCs), were significantly up-regulated. In contrast, components of the complement system, chemokines, chemokine receptors, and transcription factors crucial for regulating inflammatory processes were among the genes most down-regulated. Consistently, we found that the level of myocardin, a key transcription factor promoting contractile SMC phenotype, was greatly increased, and the proinflammatory transcription factors NFκB1 and CCAAT/enhancer-binding protein β were significantly attenuated in V3-expressing SMCs. Overall, these findings demonstrate that V3 expression reprograms ASMCs promoting differentiated and anti-inflammatory phenotypes.
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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.