Pancreatic β-Cell Death in Response to Pro-Inflammatory Cytokines Is Distinct from Genuine Apoptosis 英文参考文献.docVIP

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Pancreatic β-Cell Death in Response to Pro-Inflammatory Cytokines Is Distinct from Genuine Apoptosis 英文参考文献.doc

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Pancreatic β-Cell Death in Response to Pro-Inflammatory Cytokines Is Distinct from Genuine Apoptosis 英文参考文献

Pancreaticb-CellDeathinResponsetoPro-Inflammatory CytokinesIsDistinctfromGenuineApoptosis J.JasonCollier1,4*,SusanJ.Burke1,MaryE.Eisenhauer2,DanhongLu3,ReneeC.Sapp1,CarlieJ. Frydman1,ShawnR.Campagna2,4 1Department of Nutrition, University of Tennessee, Knoxville, Tennessee, United States of America, 2Department of Chemistry, University of Tennessee, Knoxville, Tennessee,UnitedStatesofAmerica,3SarahW.StedmanNutritionandMetabolismCenter,DukeUniversityMedicalCenter,Durham,NorthCarolina,UnitedStatesof America,4UniversityofTennesseeObesityResearchCenter,Knoxville,Tennessee,UnitedStatesofAmerica Abstract Areductioninfunctionalb-cellmassleadstobothmajorformsofdiabetes;pro-inflammatorycytokines,suchasinterleukin- 1beta(IL-1b)andgamma-interferon(c-IFN),activatesignalingpathwaysthatdirectpancreaticb-celldeathanddysfunction. However, the molecular mechanism of b-cell death in this context is not well understood. In this report, we tested the hypothesisthatindividualcellulardeathpathwaysdisplaycharacteristicphenotypesthatallowthemtobedistinguishedby theprecisebiochemicalandmetabolicresponsesthatoccurduringstimulus-specificinitiation.Using832/13andINS-1Erat insulinomacellsandisolatedratislets,weprovideevidencethatapoptosisisunlikelytobetheprimarypathwayunderlying b-cell death in response to IL-1b+c-IFN. This conclusion was reached via the experimental results of several different interdisciplinarystrategies,whichincluded:1)tandemmassspectrometrytodelineatethemetabolicdifferencesbetween IL-1b+c-IFNexposureversusapoptoticinductionbycamptothecinand2)pharmacologicalandmolecularinterferencewith either NF-kB activity or apoptosome formation. These approaches provided clear distinctions in cell death pathways initiated by pro-inflammatory cytokines and bona fide inducers of apoptosis. Collectively, the results reported herein demonstrate that pancreatic b-cells undergo apoptosis in response to camptothecin or staurosporine, but not pro- inflammatorycytokines. Citation: Collier JJ,Bur