ArticleMediators of inflammation2013
Nitric oxide is a mediator of antiproliferative effects induced by proinflammatory cytokines on pancreatic beta cells.
Article in Mediators of inflammation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 29 citations in OpenAlex.
- Preventing the onset of diabetes with precision delivery of mesenchymal stem cells to the pancreas in a preclinical model.Stem cell research & therapy · 2025Article
- Oxidative stress-mediated beta cell death and dysfunction as a target for diabetes management.Frontiers in endocrinology · 2022Review
- Article
- Good Cop, Bad Cop: The Opposing Effects of Macrophage Activation State on Maintaining or Damaging Functional β-Cell Mass.Metabolites · 2020Review
- The Role of Endothelial Dysfunction in Peripheral Blood Nerve Barrier: Molecular Mechanisms and Pathophysiological Implications.International journal of molecular sciences · 2019Review
- Oxidative stress and antioxidant treatment in patients with peripheral artery disease.Physiological reports · 2018Review
- Early blood pressure alterations are associated with pro-inflammatory markers in type 1 diabetes mellitus.Journal of human hypertension · 2017Observational
- Survival of encapsulated islets: More than a membrane story.World journal of transplantation · 2016Review
- Effect and mechanisms of human Wharton's jelly-derived mesenchymal stem cells on type 1 diabetes in NOD model.Endocrine · 2015Article
- Comparison of inducible nitric oxide synthase activity in pancreatic islets of young and aged rats.Iranian journal of basic medical sciences · 2015Article
- Article
- Nitric Oxide Synthase is Necessary for Normal Urogenital Development.Andrology : open access · 2013Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nitric oxide (NO) is involved in several biological processes. In type 1 diabetes mellitus (T1DM), proinflammatory cytokines activate an inducible isoform of NOS (iNOS) in β cells, thus increasing NO levels and inducing apoptosis. The aim of the current study is to determine the role of NO (1) in the antiproliferative effect of proinflammatory cytokines IL-1 β , IFN- γ , and TNF- α on cultured islet β cells and (2) during the insulitis stage prior to diabetes onset using the Biobreeding (BB) rat strain as T1DM model. Our results indicate that NO donors exert an antiproliferative effect on β cell obtained from cultured pancreatic islets, similar to that induced by proinflammatory cytokines. This cytokine-induced antiproliferative effect can be reversed by L-NMMA, a general NOS inhibitor, and is independent of guanylate cyclase pathway. Assays using NOS isoform specific inhibitors suggest that the NO implicated in the antiproliferative effect of proinflammatory cytokines is produced by inducible NOS, although not in an exclusive way. In BB rats, early treatment with L-NMMA improves the initial stage of insulitis. We conclude that NO is an important mediator of antiproliferative effect induced by proinflammatory cytokines on cultured β cell and is implicated in β -cell proliferation impairment observed early from initial stage of insulitis.
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