کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5906239 | 1159967 | 2013 | 6 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Heat shock transcription factor 1 attenuates TNFα-induced cardiomyocyte death through suppression of NFκB pathway
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کلمات کلیدی
TNFαRHDNLSHSF1hsp70HSP90Jnkc-Jun N-terminal protein kinase - C-Jun N-terminal protein kinaseNFκB - NFKBtumor necrosis factor alpha - تومور نکروز عامل آلفاRel homology domain - دامنه هماهنگی RelRelA - رالاnuclear localization signal - سیگنال محلی سازی هسته ایHeat shock transcription factor 1 - فاکتور رونویسی شوک حرارت 1nuclear factor-κB - فاکتور هسته ای κBpolymerase chain reaction - واکنش زنجیره ای پلیمرازPCR - واکنش زنجیرهٔ پلیمرازHeat shock proteins 70 - پروتئین شوک حرارت 70
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
ژنتیک
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Heat shock transcription factor 1 (HSF1), which has been identified as an endogenous cardioprotective factor, possesses potent anti-inflammatory effects. However, the underlying mechanisms have not been fully understood yet. In this study, we investigated the effects of HSF1-regulated RelA, a subunit of NFκB on cardiomyocyte death. Cultured cardiomyocytes were transfected with HSF1 plasmid before the treatment of TNFα. Cell death ratio was determined by cell staining. Additionally, the expression of RelA in the cytoplasm and cytonucleus as well as its subcellular location was detected, and the expression of heat shock proteins (HSP70 and HSP90) in the cardiomyocytes was also examined. Not only did TNFα remarkably enhanced cardiac cell death, but also elevated the expressions of intracellular RelA and elicited its translocation. Overexpression of HSF1 effectively attenuated cell death induced by TNFα. Although HSF1 didn't significantly inhibit the intracellular activation of RelA induced by TNFα at an early stage, HSF1 decreased the levels of RelA and the translocation of RelA in the cytoplasm and cell nucleus at late stage. Besides, the expression of HSP70 and HSP90 was significantly increased when HSF1 was overexpressed. These results suggested that HSF1 attenuated cardiomyocyte death via inhibiting activation of RelA as well as preventing its translocation from the cytoplasm to the cytonucleus, which was partially associated with HSP70 and HSP90 up-regulated by HSF1 overexpression.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Gene - Volume 527, Issue 1, 15 September 2013, Pages 89-94
Journal: Gene - Volume 527, Issue 1, 15 September 2013, Pages 89-94
نویسندگان
Lianpin Wu, Chaohui Hu, Mingyuan Huang, Minghua Jiang, Lingyan Lu, Jifei Tang,