Exogenous ARC down-regulates caspase-3 expression and inhibits apoptosis of broiler chicken cardiomyocytes exposed to hydrogen peroxide
文献类型: 外文期刊
作者: Wu, Liming 1 ; Xi, Zhaofang 1 ; Guo, Rui 2 ; Liu, Songrui 1 ; Yang, Shijin 1 ; Liu, Dongyang 1 ; Dong, Shiqi 1 ; Guo, Din 1 ;
作者机构: 1.Huazhong Agr Univ, Dept Vet Internal Med, Coll Vet Med, Wuhan 430070, Peoples R China
2.Hubei Acad Agr Sci, Hubei Key Lab Anim Embryo & Mol Breeding, Wuhan 430070, Peoples R China
期刊名称:AVIAN PATHOLOGY ( 影响因子:3.378; 五年影响因子:3.237 )
ISSN: 0307-9457
年卷期: 2013 年 42 卷 1 期
页码:
收录情况: SCI
摘要: Apoptosis repressor with caspase recruitment domain (ARC) is highly involved in apoptosis induced by oxidative stress or ischaemia/reperfusion injury. Furthermore, even though the exact mechanism is still unknown, some studies suggest that exogenous ARC also possesses anti-apoptotic ability. The study investigated whether mouse-derived ARC acquires anti-apoptotic ability and the pathway of regulation in chick embryo cardiomyocytes. To evaluate whether mouse-derived ARC can inhibit chick embryo cardiomyocyte apoptosis induced by hydrogen peroxide, recombinant pcDNA3.1/ARC plasmid was acquired and transfected into chick embryo cardiomyocytes. ARC-related gene (caspase-2, caspase-8, caspase-3, and caspase-9, cytochrome C, bcl-2, and XIAP) mRNA and protein expression levels were detected by real-time polymerase chain reaction and western blotting, respectively. Here we demonstrate that hydrogen peroxide induced apoptosis in chick embryo cardiomyocytes in a time-dependent manner and that this effect could be suppressed by mouse-derived ARC expression. Moreover, unlike endogenous ARC, exogenous ARC was exclusively expressed in the cytoplasm and down-regulated caspase-2, caspase-8, and caspase-3, bcl-2, and XIAP gene expression levels. However, only caspase-3 protein levels were decreased. In addition, threonine 149 phosphorylation by CK2 was required for exogenous ARC to exert an anti-apoptotic effect in chicken embryo cardiomyocytes and suggested exogenous ARC may in part share the same pathway of regulation with endogenous ARC. These results indicate that mouse-derived ARC plays an important role in protection of chick embryo cardiomyocytes against oxidative stress apoptosis by inhibiting caspase-3 mRNA and protein expression levels.
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