ArticleCell cycle (Georgetown, Tex.)2012
TNF-α-mediated proliferation of vascular smooth muscle cells involves Raf-1-mediated inactivation of Rb and transcription of E2F1-regulated genes.
Article in Cell cycle (Georgetown, Tex.), 2012. 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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Who cites it
26 citing papers in PubMed.
- Single-cell transcriptomics reveals NDRG1/TGF‑β1 associated vascular smooth muscle cell phenotypic switching in chronic thromboembolic pulmonary hypertension.Journal of thrombosis and thrombolysis · 2026Article
- Delivery of Superoxide Dismutase 3 Gene with Baculoviruses Inhibits TNF-α Triggers Vascular Smooth Muscle Cell Proliferation and Inflammation.Current gene therapy · 2025Article
- Polymorphism-driven immune disruptions in Kawasaki disease across populations: decoding the role of T and B-cells.Frontiers in immunology · 2025Review
- Physiology and Pathobiology of Perivascular Adipose Tissue: Inflammation-based Atherogenesis.Physiological research · 2024Review
- Review
- Inflammatory Mediators in Atherosclerotic Vascular Remodeling.Frontiers in cardiovascular medicine · 2022Review
- The Effect of TNF-Cardiology research and practice · 2022Review
- Anti-Atherosclerotic Effect of Gossypetin on Abnormal Vascular Smooth Muscle Cell Proliferation and Migration.Antioxidants (Basel, Switzerland) · 2021Article
- Cytokines as therapeutic targets for cardio- and cerebrovascular diseases.Basic research in cardiology · 2021Review
- TNFα and Reactive Oxygen Signaling in Vascular Smooth Muscle Cells in Hypertension and Atherosclerosis.American journal of hypertension · 2020Review
- Tumor Necrosis Factor Induces Obliterative Pulmonary Vascular Disease in a Novel Model of Connective Tissue Disease-Associated Pulmonary Arterial Hypertension.Arthritis & rheumatology (Hoboken, N.J.) · 2020Article
- Sirtuin 1 reduces hyaluronan synthase 2 expression by inhibiting nuclear translocation of NF-κB and expression of the long-noncoding RNA HAS2-AS1.The Journal of biological chemistry · 2020Article
- TiOACS biomaterials science & engineering · 2020Article
- RECK suppresses interleukin-17/TRAF3IP2-mediated MMP-13 activation and human aortic smooth muscle cell migration and proliferation.Journal of cellular physiology · 2019Article
- Restoring extracellular matrix synthesis in senescent stem cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- A new CHO (Chinese hamster ovary)-derived cell line expressing anti-TNFα monoclonal antibody with biosimilar potential.Immunologic research · 2018Article
- Review
- Gene expression profiles and signaling mechanisms in αBMC systems biology · 2017Article
- NANOG Restores Contractility of Mesenchymal Stem Cell-Based Senescent Microtissues.Tissue engineering. Part A · 2017Article
- Tumor necrosis factor alpha derived from classically activated "M1" macrophages reduces interstitial cell of Cajal numbers.Neurogastroenterology and motility · 2017Article
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
Atherosclerosis is characterized by hyperplastic neointima and an inflammatory response with cytokines such as TNFα. TNFα is a pleiotropic cytokine that mediates inflammatory, proliferative, cytostatic and cytotoxic effects in a variety of cell types, including endothelial cells and vascular smooth muscle cells (VSMCs). Interestingly, TNFα has been shown to play two very opposing roles in these cell types; it inhibits proliferation and induces apoptosis in endothelial cells, while it enhances the proliferation and migration of VSMCs. Here we show that TNFα is capable of stimulating proliferation of rat VSMCs as well as human VSMCs in a Raf-1/MAP K-dependent manner. TNFα could increase the expression of E2F-regulated proliferative cdc6, Thymidylate synthase (TS) and cdc25A genes in Aortic smooth muscle cells (AoSMC), as seen by real time PCR assays. There is an activation of the stress-induced kinase, JNK1, in VSMCs upon TNFα stimulation. TNFα was capable of inducing binding of the Raf-1 kinase to Rb, and treatment with the Rb-Raf-1 inhibitor, RRD-251, could prevent TNFα-induced S-phase entry in AoSMCs. In addition, inhibition of Raf-1 or Src kinases using pharmacologic inhibitors could also prevent S-phase entry, while inhibition of JNK was not as effective. These results suggest that inhibiting the Rb-Raf-1 interaction is a potential avenue to prevent VSMC proliferation associated with atherosclerosis.
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