Paper Information

Journal:   IRANIAN JOURNAL OF BASIC MEDICAL SCIENCES   AUGUST 2013 , Volume 16 , Number 8; Page(s) 928 To 935.
 
Paper: 

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

 
 
Author(s):  MURTAZA IRAM*, WANG HONG XIA, MUSHTAQ SOBIA, JAVED QAMAR, LI PEI FENG
 
* DEPARTMENT OF BIO-CHEMSITRY, FACULTY OF BIOLOGICAL SCIENCES, QUAID-I-AZAM UNIVERSITY ISLAMABAD, 45320, ISLAMABAD, PAKISTAN
 
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.

 
Keyword(s): APOPTOSIS REPRESSOR WITH, CASPASE RECRUITMENT DOMAIN, CARDIMYOCYTE HYPERTROPHY, ENDOTHELIN-1, PROTEIN KINASE CK2, REACTIVE OXYGEN SPECIES
 
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