Diabetic β-Cells Can Achieve Self-Protection against Oxidative Stress through an Adaptive Up-Regulation of Their Antioxidant Defenses 英文参考文献.docVIP

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Diabetic β-Cells Can Achieve Self-Protection against Oxidative Stress through an Adaptive Up-Regulation of Their Antioxidant Defenses 英文参考文献.doc

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Diabetic β-Cells Can Achieve Self-Protection against Oxidative Stress through an Adaptive Up-Regulation of Their Antioxidant Defenses 英文参考文献

Diabeticb-CellsCanAchieveSelf-Protectionagainst OxidativeStressthroughanAdaptiveUp-Regulationof TheirAntioxidantDefenses Gre′goryLacraz1,FlorenceFigeac1,JamilehMovassat1,NadimKassis2,JosianeCoulaud1,AnneGalinier3, CorinneLeloup3,DanielleBailbe′1,Franc?oiseHomo-Delarche1,BernardPortha1* 1EquipeB2PE(BiologieetPathologieduPancre′asEndocrine),Unite′ BFA(BiologieFonctionnelleetAdaptative),Universite′ Paris-DiderotetCNRSEAC7059,Paris,France, 2EquipeHERGE,Unite′ BFA(BiologieFonctionnelleetAdaptative),Universite′ Paris-DiderotetCNRSEAC7059,Paris,France,3UMR5241,CNRSandUniversite′ P.Sabatier, CHURangueil,Toulouse,France Abstract Background: Oxidative stress (OS), through excessive and/or chronic reactive oxygen species (ROS), is a mediator of diabetes-relateddamagesinvarioustissuesincludingpancreaticb-cells.Here,wehaveevaluatedisletOSstatusandb-cell responsetoROSusingtheGK/Parratasamodeloftype2diabetes. Methodology/Principal Findings: Localization of OS markers was performed on whole pancreases. Using islets isolated from 7-day-old or 2.5-month-old male GK/Par and Wistar control rats, 1) gene expression was analyzed by qRT-PCR; 2) insulinsecretionrate wasmeasured;3)ROS accumulationandmitochondrial polarizationwereassessed byfluorescence methods; 4) antioxidant contents were quantified by HPLC. After diabetes onset, OS markers targeted mostly peri-islet vascular and inflammatory areas, and not islet cells. GK/Par islets revealed in fact protected against OS, because they maintained basal ROS accumulation similar or even lower than Wistar islets. Remarkably, GK/Par insulin secretion also exhibited strong resistance to the toxic effect of exogenous H2O2 or endogenous ROS exposure. Such adaptation was associated to both high glutathione content and overexpression (mRNA and/or protein levels) of a large set of genes encodingantioxidantproteinsaswellasUCP2.Finally,weshowedthatsuchaphenotypewasnotinnatebutspontaneously acquiredafterdiabetesonset,astheresultofanad