1. TGF-β1 activates the canonical NF-κB signaling to promote cell survival and proliferation in dystrophic muscle fibroblasts in vitro.
- Author
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Ma, Zhen-Yu, Zhong, Zhi-Gang, Qiu, Meng-Yao, Zhong, Yu-Hua, and Zhang, Wei-Xi
- Subjects
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TRANSFORMING growth factors , *NF-kappa B , *CELL proliferation , *MUSCLE dysmorphia , *FIBROBLASTS , *IN vitro studies , *LABORATORY mice - Abstract
Activated fibroblasts continue to proliferate at injury sites, leading to progressive muscular fibrosis in Duchenne muscular dystrophy (DMD). TGF-β1 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-β1 increased the resistance to apoptosis and stimulated cell cycle progression in dystrophic muscle fibroblasts under serum deprivation conditions in vitro . TGF-β1 treatment activated the canonical NF-κB pathway; and we found that pharmacological inhibition of IKKβ with IMD-0354 and RelA gene knockdown with siRNA attenuated these effects of TGF-β1 on dystrophic muscle fibroblasts. Collectively, our data suggest that TGF-β1 prevents apoptosis and cell cycle arrest in dystrophic muscle fibroblasts through the canonical NF-κB signaling pathway. [ABSTRACT FROM AUTHOR]
- Published
- 2016
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