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نویسندگان مقالات پربازدید :
بیوشیمی مولکولی و سلولی 2013
جزئیات رویداد
اینستاگرام تی پی بین
همایش ، رویداد ، ژورنال
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  • nf-κb-mediated mir-30b regulation in cardiomyocytes cell death by targeting bcl-2

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    • تاریخ ارائه: 1392/07/24
    • تاریخ انتشار در تی پی بین: 1392/07/24
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    • شماره تماس دبیرخانه رویداد: -
     angiotensin ii(ang ii)-stimulated cardiomyocytes hypertrophy and apoptosis are associated with nuclear factor-κb (nf-κb) activation. nf-κb, a redox-sensitive transcription factor, contributes a critical role in cell death, but, ang ii-stimulated nf-κb-mediated cardiomyocytes apoptosis remains less understood. recently, micrornas (mirnas) have been shown to be critical regulators in various cardiac remodeling processes; however, nf-κb-mediated mirna’s role in cardiomyocytes apoptosis remains undetermined. the mir-30b has been implicated in diverse cardiac remodeling; but, nf-κb-mediated mir-30b modulation in ang ii-induced cardiomyocytes death is currently unknown. in the present study, neonatal cardiomyocytes were pretreated with sn50, a selective cell permeable peptide inhibitor of nf-κb, or transfected with mir-30b mimetic and inhibitors separately, and then challenged with ang ii. the target gene, bcl-2, and nf-κb transcriptional activity were analyzed. our results demonstrated that nf-κb positively regulated mir-30b expression in ang ii-induced cardiomyocytes apoptosis, and bcl-2 was a direct target for mir-30b. nf-κb further regulated the expression of bcl-2 in the above setting. furthermore, ang ii-induced cardiomyocytes apoptosis rescued by inhibiting either nf-κb or mir-30b provided an important role in cardiomyocytes cell death. we evaluated a critical role of nf-κb-mediated mir-30b modulation in ang ii-stimulated cardiomyocytes targeting bcl-2. our data may provide a new insight of mir-30b’s role in myocardial infarction or ischemia.

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