小窝蛋白-3在PKC Eplison亚型介导缺血预适应心脏保护中的作用机制  

Ischemic preconditioning promotes association of protein kinase C isoforms with caveolin-3 in cardiac myocytes

作　　者：遇红梅[1] 吕晓明[1] 杨宇丹[1] 孙巍[1] 潘肃[1] 

机构地区：[1]吉林大学中日联谊医院输血科,吉林长春130033

出　　处：《中国生物制品学杂志》2013年第11期1580-1584,共5页Chinese Journal of Biologicals

基　　金：吉林省科技发展计划青年科研项目(20130522032JH)

摘　　要：目的探讨小窝蛋白-3(caveolin-3,Cav-3)在蛋白激酶C(protein kinase C,PKC)Eplison亚型(PKCε)介导缺血预适应心脏保护中的作用机制。方法将大鼠心肌细胞置于密闭容器中进行诱导缺氧,建立缺血预适应模型,通过Western blot、荧光共振能量转移法(fluorescence resonance energy transfer,FRET)检测PKC 5种亚型在缺血预适应后的变化,判断Cav-3与PKCε表达、转位及活化的相关性。结果缺血预适应后,PKCε、PKCδ、PKCα选择性转位到富含Cav的浆膜上,但不包括PKCβ1和PKCζ。缺血预适应增加了FRET信号,促进PKCε转位到富含Cav浆膜上及增加Cav-3与PKCε蛋白的偶联量。结论缺血预适应可能直接通过Cav-3促进PKCε、PKCδ、PKCα与心肌细胞富含Cav浆膜微小结构域的联系,这种调节机制在心肌保护中起重要作用。Objective To investigate the possible mechanisms of caveolin -3 （Cav-3） in protein kinase C （PKC） isoforms mediated cardioprotection of ischemic preconditioning. Methods Hypoxia of adult rat cardiac myocytes （ARCM） were in-duced in a closed container to establish a cell model of hypoxic preconditioning. The changes of five PKC isoforms, PKCα,PKCβ1, PKCε,PKCδ and PKCζ,before and after ischemic preconditioning were determined by Western blot and fluorescence resonance energy transfer （FRET）, based on which the relationship of Cav-3 to the expression,translocation and activation of PKC was evaluated. Results Western blot indicated the selective translocations of PKCε,PKCδ and PKCα, but not PKCβ1 or PKCζ, onto the Cav-riched plasma membrane. The ischemic preconditioning enhanced the FRET signal, promoted the translocation of PKCε to the Cav-rich plasma membrane, and increased the coupling level of Car-3 to PKCε. Conclusion Ischemic preconditioning might promote the associations of PKCε,PKCδ and PKCζ with the Car-rich plasma membrane microdomain of cardiac myocytes possibly via direct molecular interaction with Cav-3,which plays an important role in cardioprotection.

关 键 词：小窝蛋白-3 蛋白激酶C 缺血预适应 心肌细胞 

分 类 号：R541[医药卫生—心血管疾病]