ArticleThe Journal of biological chemistry2014
Expression of versican V3 by arterial smooth muscle cells alters tumor growth factor β (TGFβ)-, epidermal growth factor (EGF)-, and nuclear factor κB (NFκB)-dependent signaling pathways, creating a microenvironment that resists monocyte adhesion.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 28 citations in OpenAlex.
- VCAN is upregulated in the cervical cancer stroma and modulates macrophage polarization.Frontiers in oncology · 2026Article
- 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
- TGF-β1 and TGFβR2 Gene Polymorphisms in Patients with Unstable Angina.Biomedicines · 2023Article
- 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
- A role for proteoglycans in vascular disease.Matrix biology : journal of the International Society for Matrix Biology · 2018Review
- Hepatic expression profiling identifies steatosis-independent and steatosis-driven advanced fibrosis genes.JCI insight · 2018Article
- Proteoglycans as Immunomodulators of the Innate Immune Response to Lung Infection.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2018Review
- Sheep-Specific Immunohistochemical Panel for the Evaluation of Regenerative and Inflammatory Processes in Tissue-Engineered Heart Valves.Frontiers in cardiovascular medicine · 2018Article
- Provisional matrix: A role for versican and hyaluronan.Matrix biology : journal of the International Society for Matrix Biology · 2017Review
- Interplay of extracellular matrix and leukocytes in lung inflammation.Cellular immunology · 2017Review
- Versican Deficiency Significantly Reduces Lung Inflammatory Response Induced by Polyinosine-Polycytidylic Acid Stimulation.The Journal of biological chemistry · 2017Article
- Cancer Cell-derived Exosomes Induce Mitogen-activated Protein Kinase-dependent Monocyte Survival by Transport of Functional Receptor Tyrosine Kinases.The Journal of biological chemistry · 2016Article
- Inhibition of versican expression by siRNA facilitates tropoelastin synthesis and elastic fiber formation by human SK-LMS-1 leiomyosarcoma smooth muscle cells in vitro and in vivo.Matrix biology : journal of the International Society for Matrix Biology · 2016Article
- Expression of V3 Versican by Rat Arterial Smooth Muscle Cells Promotes Differentiated and Anti-inflammatory Phenotypes.The Journal of biological chemistry · 2015Article
- Proteoglycan form and function: A comprehensive nomenclature of proteoglycans.Matrix biology : journal of the International Society for Matrix Biology · 2015Review
- FACE analysis as a fast and reliable methodology to monitor the sulfation and total amount of chondroitin sulfate in biological samples of clinical importance.Molecules (Basel, Switzerland) · 2014Article
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Authors and funding
4 authors at 1 institution.
Funding
Abstract
Monocyte/macrophage accumulation plays a critical role during progression of cardiovascular diseases, such as atherosclerosis. Our previous studies demonstrated that retrovirally mediated expression of the versican V3 splice variant (V3) by arterial smooth muscle cells (ASMCs) decreases monocyte adhesion in vitro and macrophage accumulation in a model of lipid-induced neointimal formation in vivo. We now demonstrate that V3-expressing ASMCs resist monocyte adhesion by altering the composition of the microenvironment surrounding the cells by affecting multiple signaling pathways. Reduction of monocyte adhesion to V3-expressing ASMCs is due to the generation of an extracellular matrix enriched in elastic fibers and depleted in hyaluronan, and reduction of the proinflammatory cell surface vascular cell adhesion molecule 1 (VCAM1). Blocking these changes reverses the protective effect of V3 on monocyte adhesion. The enhanced elastogenesis induced by V3 expression is mediated by TGFβ signaling, whereas the reduction in hyaluronan cable formation induced by V3 expression is mediated by the blockade of epidermal growth factor receptor and NFκB activation pathways. In addition, expression of V3 by ASMCs induced a marked decrease in NFκB-responsive proinflammatory cell surface molecules that mediate monocyte adhesion, such as VCAM1. Overall, these results indicate that V3 expression by ASMCs creates a microenvironment resistant to monocyte adhesion via differentially regulating multiple signaling pathways.
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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.