Lin28B/let-7d axis contributes to pulmonary fibrosis by affecting mesenchymal phenotypic properties of lung fibroblasts
10.3969/j.issn.1001-1978.2017.02.007
- VernacularTitle:Lin28B/let-7d 环路调控成纤维细胞功能参与肺纤维化发生
- Author:
Haihai LIANG
;
Tianyu LI
;
Yan XIE
;
Hongli SHAN
- Keywords:
pulmonary fibrosis;
Lin28B;
let-7d;
MRC-5 cell;
myofibroblasts;
cell proliferation
- From:
Chinese Pharmacological Bulletin
2017;33(2):175-179,180
- CountryChina
- Language:Chinese
-
Abstract:
Aim To examine the role and uderlying mechanisms of Lin28 /let-7d axis in the proliferation of lung fibrobalsts and fibroblasts-into-myfibroblasts tran-sition,and provide novel strategy for the treatment of idiopathic pulmonary fibrosis (IPF).Methods We induced experimental lung fibrosis in mice by intratra-cheally injection of bleomycin (BLM).Ang Ⅱ and TGF-β1 were used to induce fibrogenesis in cultured MRC-5 cells;qRT-PCR and Western blot were applied to determine the changes of Lin28B,collagen 1 α1 and collagen 3α1 ;MTT assay,Edu satining and immun-ofluoresence were used to examine the cell viability, proliferation and fibroblasts-into-myofibroblasts transi-tion in MRC-5 cells.Results Lin28B was increased in the lung of mice with experimental lung fibrosis and in MRC-5 cells treated with AngⅡ or TGF-β1 .Moreo-ver,Lin28B enhanced collagen deposition via inhibi-ting expression of let-7d,which maybe contribute to the progression of IPF.In addition,further studies showed that Lin28B promoted proliferation and fibro-blasts-into-myofibroblasts in MRC-5 cells.Conclusion Lin28B /let-7d axis contributes to fibrogenesis via promotes fibroblasts-into-myofibroblasts transition, which may provide novel approaches for lung fibrosis treatment.
