Open AccessPeriostin down‐regulation attenuates the pro‐fibrogenic response of hepatic stellate cells induced by TGF ‐β1
Author(s) -
Hong Li,
Shejiao Dai,
Fenrong Chen,
Gang Zhao,
Lei Dong
Publication year - 2015
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/jcmm.12636
Subject(s) - periostin , hepatic stellate cell , matricellular protein , smad , transforming growth factor , cell growth , microbiology and biotechnology , extracellular matrix , ctgf , chemistry , cell cycle , myofibroblast , cancer research , western blot , fibrosis , growth factor , biology , cell , medicine , endocrinology , receptor , biochemistry , gene
Liver fibrosis is characterized by an exacerbated accumulation of deposition of the extracellular matrix ( ECM ), and the activation of hepatic stellate cells ( HSC ) plays a pivotal role in the development of liver fibrosis. Periostin has been shown to regulate cell adhesion, proliferation, migration and apoptosis; however, the involvement of periostin and its role in transforming growth factor ( TGF )‐β1‐induced HSC activation remains unclear. We used RT ‐ PCR and Western blot to evaluate the expression level of periostin in hepatic fibrosis tissues and HSC s, respectively. Cell proliferation was determined using the Cell Proliferation ELISA BrdU kit, cell cycle was analysed by flow cytometry. The expression of α‐smooth muscle actin (α‐ SMA ), collagen I, TGF ‐β1, p‐Smad2 and p‐Smad3 were determined by western blot. Our study found that periostin was up‐regulated in liver fibrotic tissues and activated HSC s. In addition, si RNA ‐periostin suppressed TGF ‐β1‐induced HSC proliferation. The HSC transfected with si RNA ‐periostin significantly inhibited TGF ‐β1‐induced expression levels of α‐ SMA and collagen I. Furthermore, TGF ‐β1 stimulated the expression of periostin, and si RNA ‐periostin attenuated TGF ‐β1‐induced Smad2/3 activation in HSC s. These results suggest that periostin may function as a novel regulator to modulate HSC activation, potentially by promoting the TGF ‐β1/Smad signalling pathway, and propose a strategy to target periostin for the treatment of liver fibrosis.