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首页> 外文期刊>Journal of Cellular Physiology >TGFbeta receptor activation enhances cardiac apoptosis via SMAD activation and concomitant NO release.
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TGFbeta receptor activation enhances cardiac apoptosis via SMAD activation and concomitant NO release.

机译：TGFbeta受体激活增强心脏通过SMAD激活细胞凋亡,相伴释放。

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Transforming growth factor beta (TGFbeta) expression is induced in the myocardium during transition from compensated hypertrophy to heart failure. In cardiomyocytes, stimulation with TGFbeta results in restricted contractile function and enhanced apoptosis. Nitric oxide (NO) also induces apoptosis and influences cardiac function. Therefore, we wanted to know whether NO is causally involved in TGFbeta-induced apoptosis. In isolated ventricular cardiomyocytes of adult rat incubation with TGFbeta(1) increased NO release which was inhibited by NOS inhibitor ETU but not with iNOS inhibitor (1400 W) or nNOS inhibitor (TFA). In addition, TGFbeta-induced apoptosis was blocked with ETU and ODQ, but not with 1400 W or TFA. The consequent assumption that endothelial NOS is involved in TGFbeta-induced NO formation and apoptosis was supported by increased phosphorylation of eNOS at serine 1177 and by the fact that TGFbeta did not increase NO release in eNOS KO mice. Furthermore, TGFbeta-induced apoptosis, NO formation, SMAD binding activity and SMAD2 phosphorylation were blocked by a TGFbeta receptor antagonist, but only apoptosis and NO formation could be blocked with ETU. Expression of SMAD7 was increased after TGFbeta stimulation and blocked with TGFbeta receptor antagonist but not after blocking NO synthase with ETU. Conclusion: In cardiomyocytes TGFbeta-induced apoptosis is mediated via TGFbeta receptor activation that concomitantly activates SMAD transcription factors and the eNOS/NO/sGC pathway. Both of these pathways are needed for apoptosis induction by TGFbeta. This reveals a new pathway of cardiac NO release and identifies NO as a possible contributor to heart failure progression mediated by TGFbeta.
机译：转化生长因子β(TGFbeta)表达式是诱导心肌中从补偿肥大过渡到心脏失败。TGFbeta导致限制收缩功能和增强细胞凋亡。(没有)也和凋亡的影响心脏功能。是否不存在参与TGFbeta-induced细胞凋亡。心室心肌细胞的成年老鼠孵化与TGFbeta(1)增加没有释放由NOS抑制剂抑制ETU但不是吗伊诺抑制剂(1400 W)或nNOS抑制剂(组织)。阻塞和ETU ODQ,但不是用1400 W或从教。NOS参与TGFbeta-induced没有形成细胞凋亡是由增加以挪士的磷酸化丝氨酸1177的事实TGFbeta不会增加没有释放以挪士KO小鼠。细胞凋亡,没有形成,SMAD绑定活动和SMAD2磷酸化被封锁TGFbeta受体拮抗剂,但只有细胞凋亡和ETU没有形成可以被阻塞。表达SMAD7 TGFbeta后增加与TGFbeta受体刺激和阻塞对手而不是阻塞后没有合酶ETU。通过TGFbeta TGFbeta-induced是介导细胞凋亡与此同时激活受体激活SMAD转录因子和以挪士/不/国网公司途径。细胞凋亡诱导TGFbeta。心脏没有释放和标识的新途径不可能成为贡献者心力衰竭由TGFbeta发展。

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