Activation of Protein Kinase C Delta following Cerebral Ischemia Leads to Release of Cytochrome C from the Mitochondria via Bad Pathway 英文参考文献.docVIP

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Activation of Protein Kinase C Delta following Cerebral Ischemia Leads to Release of Cytochrome C from the Mitochondria via Bad Pathway 英文参考文献.doc

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Activation of Protein Kinase C Delta following Cerebral Ischemia Leads to Release of Cytochrome C from the Mitochondria via Bad Pathway 英文参考文献

ActivationofProteinKinaseCDeltafollowingCerebral IschemiaLeadstoReleaseofCytochromeCfromthe MitochondriaviaBadPathway KunjanR.Dave1,SanjoyK.Bhattacharya3,IsabelSaul1,R.AnthonyDeFazio1,CameronDezfulian1,4, HungWenLin1,AmiP.Raval1,MiguelA.Perez-Pinzon1,2* 1Cerebral Vascular Disease Research Center, Department of Neurology, Leonard M. Miller School of Medicine, University of Miami, Miami, Florida, United States of America,2NeuroscienceProgram,LeonardM.MillerSchoolofMedicine,UniversityofMiami,Miami,Florida,UnitedStatesofAmerica, 3BascomPalmerEyeInstitute, LeonardM.MillerSchoolofMedicine,UniversityofMiami,Miami,Florida,UnitedStatesofAmerica,4DepartmentofMedicine,LeonardM.MillerSchoolofMedicine, UniversityofMiami,Miami,Florida,UnitedStatesofAmerica Abstract Background:Thereleaseofcytochromecfromthemitochondriafollowingcerebralischemiaisakeyeventleadingtocell death. The goal of the present study was to determine the mechanisms involved in post-ischemic activation of protein kinasecdelta(dPKC)thatleadtocytochromecrelease. Methods/Findings: We used a rat model of cardiac arrest as an in vivo model, and an in vitro analog, oxygen glucose deprivation(OGD)inrathippocampalsynaptosomes.CardiacarresttriggeredtranslocationofdPKCtothemitochondrial fraction at 1h reperfusion. In synaptosomes, the peptide inhibitor of dPKC blocked OGD-induced translocation to the mitochondria. We tested two potential pathways by which dPKC activation could lead to cytochrome c release: phosphorylation of phospholipid scramblase-3 (PLSCR3) and/or protein phosphatase 2A (PP2A). Cardiac arrest increased levels of phosphorlyated PLSCR3; however, inhibition of dPKC translocation failed to affect the OGD-induced increase in PLSCR3insynaptosomalmitochondriasuggestingthepost-ischemicphosphorylationofPLSCR3isnotmediatedbydPKC. InhibitionofeitherdPKCorPP2Adecreasedcytochromecreleasefromsynaptosomalmitochondria.Cardiacarrestresultsin thedephosphorylationofBadandBax,bothdownstreamtargetsofPP2Apromoti