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Iranian Journal of Basic Medical Sciences، جلد ۱۶، شماره ۸، صفحات ۹۲۸-۹۳۵
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عنوان انگلیسی Interplay of Phosphorylated Apoptosis Repressor with CARD, Casein Kinase-2 and Reactive Oxygen Species in Regulating Endothelin-1–Induced Cardiomyocyte Hypertrophy
چکیده انگلیسی مقاله Objective(s): The role of the Apoptosis repressor with caspase recruitment domain (ARC) in apoptosis and in certain hypertrophic responses has been previously investigated, but its regulation of Endothelin-1 induced cardiac hypertrophy remains unknown. The present study discusses the inhibitory role of ARC against endothelin–induced hypertrophy. Results:In present study Endothelin treated cardiomyocytes were used as a hypertrophic model, that were subsequently treated with adenovirus ARC and its mutant at different multiplicity of infections. Casein-kinase-2 inhibitors were used to produce dephosphorylated ARC and to study its effect on hypertrophy. Hypertrophy was assessed by cell surface area measurement, Atrial-natriuretic-Factor mRNA analysis and total protein assay. Reactive oxygen species analysis was carried out using the dichlorofluorescin-diacetate (DCFH-DA) assay. Over expression of ARC significantly inhibits Endothelin–induced cardiomyocyte hypertrophy. The nonphosphorylated mutant ARC (T149 A) remained unable to control endothelin–induced hypertrophy, suggesting a vital role for ARC phosphorylation in regulation of its activity. Sensitization study has been carried out to check the role of endogenous ARC using casein-kinase inhibitors. Finally, the significant role of ARC in regulating reactive oxygen species -mediated control of endothelin induced hypertrophy has also been assessed. Conclusion: Conclusively, present study showed the vital and potential therapeutic interventional role of ARC in preventing endothelin-1–induced cardiomyocyte hypertrophy. The regulation of hypertrophic pathway by ARC relies on blunting the reactive oxygen species attack. This study further suggests a mediatory role of casein-kinase-2 in Endothelin–induced hypertrophy, mainly through its phosphorylation of ARC.
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نویسندگان مقاله iram مرتضی | iram murtaza
division of cardiovascular research, national key laboratory of biomembrane and membrane biotechnology, institute of zoology, chinese academy of sciences, beijing 100080, people amp;apos;s republic of china department of biochemistry, faculty of biological sciences, quaid-i-azam university islamabad, 45320, islamabad, pakistan


hong خیا ونگ | hong xia wang
division of cardiovascular research, national key laboratory of biomembrane and membrane biotechnology, institute of zoology, chinese academy of sciences, beijing 100080, people amp;apos;s republic of china


sobia mushtaq | sobia mushtaq
department of biochemistry, faculty of biological sciences, quaid-i-azam university islamabad, 45320, islamabad, pakistan


قمر جاوید | qamar javed
department of biochemistry, faculty of biological sciences, quaid-i-azam university islamabad, 45320, islamabad, pakistan


pei feng l | pei feng l
division of cardiovascular research, national key laboratory of biomembrane and membrane biotechnology, institute of zoology, chinese academy of sciences, beijing 100080, people amp;apos;s republic of china
نشانی اینترنتی http://ijbms.mums.ac.ir/article_1352.html
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