ArticleThe Journal of clinical investigation1995
Nitric oxide mediates cytotoxicity and basic fibroblast growth factor release in cultured vascular smooth muscle cells. A possible mechanism of neovascularization in atherosclerotic plaques.
Article in The Journal of clinical investigation, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
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Who cites it
15 citing papers in PubMed, 114 citations in OpenAlex.
- Phenotypic Modulation of Macrophages and Vascular Smooth Muscle Cells in Atherosclerosis-Nitro-Redox Interconnections.Antioxidants (Basel, Switzerland) · 2021Review
- Effects of deoxynivalenol (DON) and its microbial biotransformation product deepoxy-deoxynivalenol (DOM-1) on a trout, pig, mouse, and human cell line.Mycotoxin research · 2017Article
- Cell Injury-Induced Release of Fibroblast Growth Factor 2: Relevance to Intracerebral Mesenchymal Stromal Cell Transplantations.Stem cells and development · 2015Article
- Nitric oxide deficiency in pulmonary hypertension: Pathobiology and implications for therapy.Pulmonary circulation · 2013Article
- Regulation of cell physiology and pathology by protein S-glutathionylation: lessons learned from the cardiovascular system.Antioxidants & redox signaling · 2012Review
- Signaling regulation of fetoplacental angiogenesis.The Journal of endocrinology · 2012Review
- Angiotensin II regulation of ovine fetoplacental artery endothelial functions: interactions with nitric oxide.The Journal of physiology · 2005Review
- Nitric oxide in inflammatory bowel disease: a universal messenger in an unsolved puzzle.Immunology · 2004Review
- Bacille Calmette-Guérin (BCG)-associated inflammation and fibrosis: modulation by recombinant BCG expressing interferon-gamma (IFN-gamma).Clinical and experimental immunology · 2000Article
- Nitric oxide synthase expression, enzyme activity and NO production during angiogenesis in the chick chorioallantoic membrane.British journal of pharmacology · 2000Article
- Nitric oxide inhibits wounds collagen synthesis.Molecular and cellular biochemistry · 1999Article
- Enhanced coronary vasa vasorum neovascularization in experimental hypercholesterolemia.The Journal of clinical investigation · 1998Article
- Nitric oxide induces heat-shock protein 70 expression in vascular smooth muscle cells via activation of heat shock factor 1.The Journal of clinical investigation · 1997Article
- Nitric oxide function in atherosclerosis.Mediators of inflammation · 1997Article
- Inhibition of neointimal proliferation in rabbits after vascular injury by a single treatment with a protein adduct of nitric oxide.The Journal of clinical investigation · 1995Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
To define the pathophysiological role of nitric oxide (NO) released from vascular smooth muscle cells (VSMC), we examined whether NO released from VSMC induces cytotoxicity in VSMC themselves and adjacent endothelial cells (EC) using a coculture system. Prolonged incubation with interleukin-1 (IL-1) induced large amounts of NO release and cytotoxicity in VSMC. NG-Monomethyl-L-arginine, an inhibitor of NO synthesis, inhibited both NO release and cytotoxicity induced by IL-1. In contrast, DNA synthesis in cocultured EC was not inhibited but rather stimulated by prolonged incubation with IL-1 or sodium nitroprusside (SNP), a NO donor. However, IL-1 and SNP did not stimulate but inhibited DNA synthesis in EC alone. On the other hand, conditioned medium from VSMC incubated for a long period with IL-1 or SNP stimulated DNA synthesis in EC alone. Furthermore, the concentration of basic fibroblast growth factor in the conditioned medium was increased and correlated with the degree of cytotoxicity in VSMC. These results indicate that NO released from VSMC induces VSMC death, which results in release of basic fibroblast growth factor, which then stimulates adjacent EC proliferation. Thus, NO released from VSMC may participate in the mechanism of neovascularization in atherosclerotic plaques.
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