Open AccessTransforming growth factor-β1 induces fibrosis in rat meningeal mesothelial cells via the p38 signaling pathway
Author(s) -
Xianchang Yue,
Yan Guo,
Haijun Yang,
Zhiwei Feng,
Tong Li,
Yuming Xu
Publication year - 2016
Publication title -
molecular medicine reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.727
H-Index - 56
eISSN - 1791-3004
pISSN - 1791-2997
DOI - 10.3892/mmr.2016.5411
Subject(s) - ctgf , transforming growth factor , cancer research , fibrosis , mapk/erk pathway , growth factor , connective tissue , pathology , signal transduction , mesothelial cell , medicine , biology , microbiology and biotechnology , receptor
Leptomeningeal fibrosis is important in the pathogenesis of communicating hydrocephalus following subarachnoid hemorrhage; however, the underlying mechanisms of leptomeningeal fibrosis remain largely unclear. In the present study, primary meningeal mesothelial cells (MMCs) were used as a cell model to investigate the effect of transforming growth factor‑β1 (TGF‑β1) on leptomeningeal fibrosis. Firstly, primary MMCs were isolated from rat brains and characterized by immunofluorescene, staining positive for keratin and vimentin, but negative for factor VIII. Upon TGF‑β1 treatment, MMCs were induced to express connective tissue growth factor (CTGF), an indicator of fibrosis, in a dose‑dependent manner. Furthermore, p38 mitogen‑activated protein kinase (MAPK) signaling was significantly activated by TGF‑β1. However, in the presence of a p38 MAPK inhibitor, TGF‑β1‑induced CTGF expression was markedly suppressed. Together, these data suggest that TGF‑β1 could induce fibrosis of MMCs via the p38 MAPK signaling pathway, providing a novel potential target for intervention in TGF‑β1‑induced leptomeningeal fibrosis.