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Publications (2)3.49 Total impact

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    ABSTRACT: 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.
    Avian Pathology 02/2013; 42(1):32-7. · 1.73 Impact Factor
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    ABSTRACT: The objective of this study was to characterize the levels of free radicals in serum and antioxidase activity after microcapsules were implanted into the subcutaneous space of mice. cell viability was evaluated using ao/Eb staining. serum free radicals, malondialdehyde and superoxide dismutase levels were evaluated by colorimetry analysis. the mice were divided into three groups: saline injection group (n=15), empty microcapsules injected group (n=21), encapsulated cells injected group (n=21). cell viability and serum analysis were executed at 1, 4 and 7 days post-implantation. Hydrogen peroxide and malondialdehyde levels initially increased in the recipients of the empty microcapsules, before decreasing to the basal level. However, in mice receiving the encapsulated cells, the levels were higher at the end of study. nitric oxide and superoxide dismutase increased after the implantation of microcapsules with or without the bHK-21 cells, but were not changed in response to the saline injection. the viability of the encapsulated cells was high in vivo, although some microcapsules had broken by 7 days post-implantation. these results suggest that nitric oxide plays a role in the specific response to microcapsules. the levels of free radicals rapidly increased immediately following microcapsule transplantation, but they caused only slight cellular damage before the microencapsulated cells were exposed.
    The International journal of artificial organs 05/2009; 32(4):224-31. · 1.76 Impact Factor