Regulation of fibroblast Fas expression by soluble and mechanical pro-fibrotic stimuli.

ABSTRACT: BACKGROUND:Fibroblast apoptosis is a critical component of normal repair and the acquisition of an apoptosis-resistant phenotype contributes to the pathogenesis of fibrotic repair. Fibroblasts from fibrotic lungs of humans and mice demonstrate resistance to apoptosis induced by Fas-ligand and prior studies have shown that susceptibility to apoptosis is enhanced when Fas (CD95) expression is increased in these cells. Moreover, prior work shows that Fas expression in fibrotic lung fibroblasts is reduced by epigenetic silencing of the Fas promoter. However, the mechanisms by which microenvironmental stimuli such as TGF-β1 and substrate stiffness affect fibroblast Fas expression are not well understood. METHODS:Primary normal human lung fibroblasts (IMR-90) were cultured on tissue culture plas

SUBMITTER: Dodi AE 

PROVIDER: S-EPMC5946418 | biostudies-literature | 2018 May

REPOSITORIES: biostudies-literature