TGF-β1 induces Fstl1 via the Smad3-c-Jun pathway in lung fibroblasts

American Journal of Physiology. Lung Cellular and Molecular Physiology
Xiaohong ZhengWen Ning

Abstract

Transforming growth factor (TGF)-β1 has long been regarded as a central mediator of tissue fibrosis. Follistatin-like 1 (Fstl1) is a crucial profibrotic glycoprotein that is upregulated in fibrotic lung tissues, and it promotes fibrogenesis via facilitating TGF-β signaling. Here we examined the signaling pathway by which TGF-β1 upregulates Fstl1 expression in mouse pulmonary fibroblasts. TGF-β1 regulated Fstl1 expression at both the transcriptional and translational levels. Although TGF-β1 rapidly activated the Smad, MAPK, and Akt pathways in lung fibroblasts, only Smad2/3 inhibition eliminated TGF-β1-induced Fstl1 expression. Analysis of the luciferase reporter activity identified a functional c-Jun transcription site in the Fstl1 promoter. Our results suggested a critical role for the Smad3-c-Jun pathway in the regulation of Fstl1 expression by TGF-β1 during fibrogenesis.

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Citations

Jul 10, 2020·International Journal of Molecular Sciences·Daniel Feng, Casimiro Gerarduzzi
Nov 11, 2019·Biomedicine & Pharmacotherapy = Biomédecine & Pharmacothérapie·Feifei FengWei Wang
Sep 20, 2017·Biomedicine & Pharmacotherapy = Biomédecine & Pharmacothérapie·Yunjuan NieChongyong Guo
Jun 3, 2021·Inflammation Research : Official Journal of the European Histamine Research Society ... [et Al.]·Yan WangLiang Dong
Aug 24, 2021·Frontiers in Molecular Biosciences·Caijuan HuanJianying Zhou
Oct 12, 2021·Experimental and Therapeutic Medicine·Yong XuQi Wu
Oct 28, 2021·International Journal of Radiation Biology·Yiting TangYang Jiao

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Methods Mentioned

BETA
immunoprecipitation
immunoprecipitation assay
PCR
ELISA
Assay
transfection
ChIP

Software Mentioned

Image Pro - Plus
PROMO

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