Open AccessTGF beta inhibits HGF, FGF7, and FGF10 expression in normal and IPF lung fibroblasts
Author(s) -
Correll Kelly A.,
Edeen Karen E.,
Redente Elizabeth F.,
Zemans Rachel L.,
Edelman Benjamin L.,
Danhorn Thomas,
CurranEverett Douglas,
MikelsVigdal Amanda,
Mason Robert J.
Publication year - 2018
Publication title -
physiological reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.918
H-Index - 39
ISSN - 2051-817X
DOI - 10.14814/phy2.13794
Subject(s) - fgf10 , fibroblast , extracellular matrix , lung , tgf beta signaling pathway , gene expression , pulmonary fibrosis , fibrosis , idiopathic pulmonary fibrosis , epithelium , cancer research , transforming growth factor beta , myofibroblast , medicine , transforming growth factor , biology , pathology , microbiology and biotechnology , gene , cell culture , biochemistry , genetics
TGF beta is a multifunctional cytokine that is important in the pathogenesis of pulmonary fibrosis. The ability of TGF beta to stimulate smooth muscle actin and extracellular matrix gene expression in fibroblasts is well established. In this report, we evaluated the effect of TGF beta on the expression of HGF, FGF7 (KGF), and FGF10, important growth and survival factors for the alveolar epithelium. These growth factors are important for maintaining type II cells and for restoration of the epithelium after lung injury. Under conditions of normal serum supplementation or serum withdrawal TGF beta inhibited fibroblast expression of HGF, FGF7, and FGF10. We confirmed these observations with genome wide RNA sequencing of the response of control and IPF fibroblasts to TGF beta. In general, gene expression in IPF fibroblasts was similar to control fibroblasts. Reduced expression of HGF, FGF7, and FGF10 is another means whereby TGF beta impairs epithelial healing and promotes fibrosis after lung injury.