Nitric Oxide Is a Mediator of Antiproliferative Effects Induced by Proinflammatory Cytokines on Pancreatic Beta Cells

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 th...

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Main Authors: Laura Quintana-Lopez, Manuel Blandino-Rosano, Gonzalo Perez-Arana, Alberto Cebada-Aleu, Alfonso Lechuga-Sancho, Manuel Aguilar-Diosdado, Carmen Segundo
Format: Article
Language:English
Published: Wiley 2013-01-01
Series:Mediators of Inflammation
Online Access:http://dx.doi.org/10.1155/2013/905175
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author Laura Quintana-Lopez
Manuel Blandino-Rosano
Gonzalo Perez-Arana
Alberto Cebada-Aleu
Alfonso Lechuga-Sancho
Manuel Aguilar-Diosdado
Carmen Segundo
author_facet Laura Quintana-Lopez
Manuel Blandino-Rosano
Gonzalo Perez-Arana
Alberto Cebada-Aleu
Alfonso Lechuga-Sancho
Manuel Aguilar-Diosdado
Carmen Segundo
author_sort Laura Quintana-Lopez
collection DOAJ
description 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-1β, 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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spelling doaj-art-c1617c83ad3e4da8a1332267b9c855ca2025-08-20T02:19:14ZengWileyMediators of Inflammation0962-93511466-18612013-01-01201310.1155/2013/905175905175Nitric Oxide Is a Mediator of Antiproliferative Effects Induced by Proinflammatory Cytokines on Pancreatic Beta CellsLaura Quintana-Lopez0Manuel Blandino-Rosano1Gonzalo Perez-Arana2Alberto Cebada-Aleu3Alfonso Lechuga-Sancho4Manuel Aguilar-Diosdado5Carmen Segundo6Investigation Unit, Puerta del Mar Hospital, Cadiz, SpainInvestigation Unit, Puerta del Mar Hospital, Cadiz, SpainInvestigation Unit, Puerta del Mar Hospital, Cadiz, SpainInvestigation Unit, Puerta del Mar Hospital, Cadiz, SpainPediatric Endocrinology Unit of Paediatric Service, Puerta del Mar Hospital, Cadiz, SpainEndocrinology and Nutrition Service, Puerta del Mar Hospital, 11009 Cadiz, SpainEndocrinology and Nutrition Service, Puerta del Mar Hospital, 11009 Cadiz, SpainNitric 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-1β, 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.http://dx.doi.org/10.1155/2013/905175
spellingShingle Laura Quintana-Lopez
Manuel Blandino-Rosano
Gonzalo Perez-Arana
Alberto Cebada-Aleu
Alfonso Lechuga-Sancho
Manuel Aguilar-Diosdado
Carmen Segundo
Nitric Oxide Is a Mediator of Antiproliferative Effects Induced by Proinflammatory Cytokines on Pancreatic Beta Cells
Mediators of Inflammation
title Nitric Oxide Is a Mediator of Antiproliferative Effects Induced by Proinflammatory Cytokines on Pancreatic Beta Cells
title_full Nitric Oxide Is a Mediator of Antiproliferative Effects Induced by Proinflammatory Cytokines on Pancreatic Beta Cells
title_fullStr Nitric Oxide Is a Mediator of Antiproliferative Effects Induced by Proinflammatory Cytokines on Pancreatic Beta Cells
title_full_unstemmed Nitric Oxide Is a Mediator of Antiproliferative Effects Induced by Proinflammatory Cytokines on Pancreatic Beta Cells
title_short Nitric Oxide Is a Mediator of Antiproliferative Effects Induced by Proinflammatory Cytokines on Pancreatic Beta Cells
title_sort nitric oxide is a mediator of antiproliferative effects induced by proinflammatory cytokines on pancreatic beta cells
url http://dx.doi.org/10.1155/2013/905175
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