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Calcineurin B subunit acts as a potential agent for preventing cardiac ischemia/reperfusion injury  ( SCI-EXPANDED收录)  

文献类型:期刊文献

英文题名:Calcineurin B subunit acts as a potential agent for preventing cardiac ischemia/reperfusion injury

作者:Guo, Junxia[1,2];Mi, Shengquan[2];Li, Jing[1];Liu, Wei[1];Yin, Yanxia[1];Wei, Qun[1]

第一作者:Guo, Junxia;郭俊霞

通讯作者:Wei, Q[1]

机构:[1]Beijing Normal Univ, Dept Biochem & Mol Biol, Beijing Key Lab Genet Engn Med & Biotechnol, Beijing 100875, Peoples R China;[2]Beijing Union Univ, Beijing Key Lab Bioact Subst & Funct Foods, Coll Arts & Sci, Beijing 100191, Peoples R China

第一机构:Beijing Normal Univ, Dept Biochem & Mol Biol, Beijing Key Lab Genet Engn Med & Biotechnol, Beijing 100875, Peoples R China

通讯机构:[1]corresponding author), Beijing Normal Univ, Dept Biochem & Mol Biol, Beijing Key Lab Genet Engn Med & Biotechnol, Beijing 100875, Peoples R China.

年份:2012

卷号:370

期号:1-2

起止页码:163-171

外文期刊名:MOLECULAR AND CELLULAR BIOCHEMISTRY

收录:;Scopus(收录号:2-s2.0-84867333285);WOS:【SCI-EXPANDED(收录号:WOS:000309478600017)】;

基金:This work was partially supported by the National Natural Science Foundation of China, the International Cooperation Project, the National Important Novel Medicine Research Project, and the Fundamental Research Funds for the Central Universities.

语种:英文

外文关键词:Calcineurin; CnB; Cardiomyocyte; Ischemia/reperfusion injury

摘要:Calcineurin B subunit (CnB) is the regulatory subunit of calcineurin (Cn), a Ca2+/calmodulin-dependent serine/threonine protein phosphatase. It has been reported that mice deleting the CnB gene lose nearly all Cn activity and show poor tolerance to cardiac stress; CnB gene expression is downregulated in the hearts of rats that have suffered ischemia/reperfusion (I/R) injury. Therefore, we wonder whether injection of exogenous CnB protein can prevent the rats from suffering I/R injury. In cardiomyocytes, fluorogenic labeling shows that exogenous CnB quickly enters the cell. Pretreatment of cardiomyocytes with CnB reduces apoptosis in response to hypoxia/reoxygenation injury (an in vitro model mimicking ischemia/reperfusion injury), and CsA reverses this effect by inhibiting Cn activity. Furthermore, CnB upregulates Bcl-2 and Bcl-XL expression in the process of hypoxia/reoxygenation injury, which may contribute to protecting cardiomyocytes against apoptosis. In vivo experiments shows that pretreatment with CnB improves cardiac contractile function and reduces the frequency of arrhythmias induced by global I/R injury. These findings reveal a novel function for CnB protein in cardiac stress response and suggest a possible application of CnB in coronary disease therapy.

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