TGF-β1 activates the canonical NF-κB signaling to promote cell survival and proliferation in dystrophic muscle fibroblasts in vitro
TGF-β1 activates the canonical NF-κB signaling to promote cell survival and proliferation in dystrophic muscle fibroblasts in vitro
复制标题
TGF-beta 1 激活典型的 NF-kappa B 信号传导，促进体外营养不良的肌肉成纤维细胞的细胞存活和增殖
DOI：
10.1016/j.bbrc.2016.02.029
复制
发表时间：
2016-03-18
影响因子：
3.1
通讯作者：
Zhang, Wei-Xi
中科院分区：
文献类型：
--
作者：
Ma, Zhen-Yu;Zhong, Zhi-Gang;Zhang, Wei-Xi
激活的成纤维细胞继续在损伤部位增殖，导致Duchenne肌营养不良症(DMD)的进行性肌肉纤维化。转化生长因子-β1是一种主要的促纤维化介质，被认为在肌肉纤维化中起着关键作用；然而，其涉及的机制尚不完全清楚。在此，我们发现在血清剥夺条件下，转化生长因子-β1在体外增加了营养不良肌成纤维细胞的抗凋亡能力，并刺激了细胞周期进程。我们发现，用IMD-0354抑制IMP和用siRNA敲除relA基因可以减弱转化生长因子-β1对营养不良肌成纤维细胞的这些作用。总之，我们的数据表明，转化生长因子-β1通过典型的核因子-kappa B信号通路阻止营养不良肌肉成纤维细胞的凋亡和细胞周期停滞。(C)2016 Elsevier Inc.保留所有权利。
Activated fibroblasts continue to proliferate at injury sites, leading to progressive muscular fibrosis in Duchenne muscular dystrophy (DMD). TGF-beta 1 is a dominant profibrotic mediator thought to play a critical role in muscle fibrosis; however, the implicated mechanisms are not fully understood. Here we showed that TGF-beta 1increased the resistance to apoptosis and stimulated cell cycle progression in dystrophic muscle fibroblasts under serum deprivation conditions in vitro. TGF-beta 1 treatment activated the canonical NF-kappa B pathway; and we found that pharmacological inhibition of IMP with IMD-0354 and RelA gene knockdown with siRNA attenuated these effects of TGF-beta 1 on dystrophic muscle fibroblasts. Collectively, our data suggest that TGF-beta 1 prevents apoptosis and cell cycle arrest in dystrophic muscle fibroblasts through the canonical NF-kappa B signaling pathway. (C) 2016 Elsevier Inc. All rights reserved.