INTERPLAY OF PHOSPHORYLATED APOPTOSIS REPRESSOR WITH CARD, CASEIN KINASE-2 AND REACTIVE OXYGEN SPECIES IN REGULATING ENDOTHELIN-1–INDUCED CARDIOMYOCYTE HYPERTROPHY

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MURTAZA IRAM; WANG HONG XIA; MUSHTAQ SOBIA; JAVED QAMAR; LI PEI FENG

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Journal Paper

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Journal: Iranian Journal of Basic Medical Sciences Year:2013 | Volume:16 | Issue:8 Page(s): 928-935

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Title

INTERPLAY OF PHOSPHORYLATED APOPTOSIS REPRESSOR WITH CARD, CASEIN KINASE-2 AND REACTIVE OXYGEN SPECIES IN REGULATING ENDOTHELIN-1–INDUCED CARDIOMYOCYTE HYPERTROPHY

Author(s)

Keywords

APOPTOSIS REPRESSOR WITH

CASPASE RECRUITMENT DOMAIN

CARDIMYOCYTE HYPERTROPHY

ENDOTHELIN-1

PROTEIN KINASE CK2

REACTIVE OXYGEN SPECIES

Abstract

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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APA: Copy

MURTAZA, IRAM, WANG, HONG XIA, MUSHTAQ, SOBIA, JAVED, QAMAR, & LI, PEI FENG. (2013). INTERPLAY OF PHOSPHORYLATED APOPTOSIS REPRESSOR WITH CARD, CASEIN KINASE-2 AND REACTIVE OXYGEN SPECIES IN REGULATING ENDOTHELIN-1–INDUCED CARDIOMYOCYTE HYPERTROPHY. IRANIAN JOURNAL OF BASIC MEDICAL SCIENCES, 16(8), 928-935. SID. https://sid.ir/paper/629665/en

Vancouver: Copy

MURTAZA IRAM, WANG HONG XIA, MUSHTAQ SOBIA, JAVED QAMAR, LI PEI FENG. INTERPLAY OF PHOSPHORYLATED APOPTOSIS REPRESSOR WITH CARD, CASEIN KINASE-2 AND REACTIVE OXYGEN SPECIES IN REGULATING ENDOTHELIN-1–INDUCED CARDIOMYOCYTE HYPERTROPHY. IRANIAN JOURNAL OF BASIC MEDICAL SCIENCES[Internet]. 2013;16(8):928-935. Available from: https://sid.ir/paper/629665/en

IEEE: Copy

IRAM MURTAZA, HONG XIA WANG, SOBIA MUSHTAQ, QAMAR JAVED, and PEI FENG LI, “INTERPLAY OF PHOSPHORYLATED APOPTOSIS REPRESSOR WITH CARD, CASEIN KINASE-2 AND REACTIVE OXYGEN SPECIES IN REGULATING ENDOTHELIN-1–INDUCED CARDIOMYOCYTE HYPERTROPHY,” IRANIAN JOURNAL OF BASIC MEDICAL SCIENCES, vol. 16, no. 8, pp. 928–935, 2013, [Online]. Available: https://sid.ir/paper/629665/en

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