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首页> 外文期刊>Journal of Cellular Physiology >Analysis of p53 and NF-kappaB signaling in modulating the cardiomyocyte fate during hypertrophy.
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Analysis of p53 and NF-kappaB signaling in modulating the cardiomyocyte fate during hypertrophy.

机译：分析p53和NF-kappaB信号调节心肌细胞的命运肥大。

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Cardiac hypertrophy leading to eventual heart failure is the most common cause of mortality throughout the world. The triggering mechanisms for cardiac hypertrophy are not clear but both apoptosis and cell proliferation have been reported in sections of failing hearts. In this study, we utilized both angiotensin II (AngII) treatment of cardiomyocytes and aortic ligation in rats (Rattus norvegicus, Wistar strain) for induction of hypertrophy to understand the cellular factors responsible for activation of apoptotic or anti-apoptotic pathway. Hypertrophy markers (ANF, beta-MHC), apoptotic proteins (Bax, Bad, Fas, p53, caspase-3, PARP), and anti-apoptotic or cell proliferation marker proteins (Bcl2, NF-kappaB, Ki-67) were induced significantly during hypertrophy, both in vitro as well as in vivo. Co-localization of both active caspase-3 and Ki-67 was observed in hypertrophied myocytes. p53 and NF-kappaBp65 binding to co-activator p300 was also increased in AngII treated myocytes. Inhibition of p53 resulted in downregulation of apoptosis, NF-kappaB activation, and NF-kappaB-p300 binding; however, NF-kappaB inhibition did not inhibit apoptosis or p53-p300 binding. Blocking of either p53 or NF-kappaB by specific inhibitors resulted in decrease in cell proliferation and hypertrophy markers, suggesting that p53 initially binds to p300 and then this complex recruits NF-kappaB. Thus, these results indicate the crucial role of p53 in regulating both apoptotic and cell proliferation during hypertrophy.
机译：心脏肥大导致最终的心失败是死亡的最常见原因在整个世界。但对于心脏肥大不清楚细胞凋亡和细胞增殖在没有心的部分。研究中,我们利用两个血管紧张素ⅱ(AngII)治疗心肌细胞和主动脉结扎在老鼠(鼠形,纯种菌株)诱导的肥大理解细胞因子激活负责凋亡和抗凋亡途径。标记(曾帮工,beta-MHC),凋亡蛋白(伯灵顿,不好,Fas, p53、caspase-3 PARP),抗凋亡和细胞增殖标记蛋白质(Bcl2 NF-kappaB, ki - 67)诱导明显肥大,体外以及体内。积极观察caspase-3和ki - 67肥大细胞。绑定co-activator p300也增加在AngII细胞治疗。的差别导致了对这些基因的细胞凋亡,NF-kappaB激活,NF-kappaB-p300绑定;然而,NF-kappaB抑制不抑制细胞凋亡或p53-p300绑定。p53或NF-kappaB特定抑制剂了在细胞增殖减少和肥大标记,表明p53最初结合p300 NF-kappaB然后这个复杂的新兵。因此,这些结果表明的至关重要的作用p53在调节凋亡和细胞在增殖肥大。

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