Author/Authors :
Dai, Yu-heng Hangzhou Women’s Hospital, Hangzhou, China , Li, Xiao-qing Second Hospital of Yingzhou District, Ningbo, China , Dong, Da-peng The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China , Gu, Hai-bo Gu The Fourth Affiliated Hospital - School of Medicine - Zhejiang University, Yiwu, China , Kong, Cheng-ying The Fourth Affiliated Hospital - School of Medicine - Zhejiang University, Yiwu, China , Xu, Zhihao The Fourth Affiliated Hospital - School of Medicine - Zhejiang University, Yiwu, China
Abstract :
Pulmonary fibrosis (PF), a progressive and life-threatening pulmonary disease, is the main pathological basis of interstitial lung
disease (ILD) which includes the idiopathic pulmonary fibrosis (IPF). No effective therapeutic strategy for pulmonary fibrosis has
been established. TGF-β signaling has emerged as the vital regulator of PF; however, the detailed molecular mechanisms of TGF-β
in PF were uncertain. In the present study, we proved that inhibition of MTORC2 suppresses the expression of P27 in MRC5 and
HLF cells. and in bleomycin-induced PF model, the expression of α-SMA and P27 was upregulated. Moreover, TGF-β application
increased the level of α-SMA, vimentin, and P27 in MRC5 and HLF cells. Furthermore, P27 overexpression advanced the cell cycle
process and promoted the proliferation of MRC5 and HLF cells. Finally, the rescue experiment showed that MTORC2 knockdown
reversed P27 overexpression-induced cell cycle acceleration and proliferation. +us, our results suggest that P27 is involved in
TGF-β-mediated PF, which was regulated by MTORC2, providing a novel insight into the development of PF.
