Abstract:
: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.
journal_name
Mol Med Repjournal_title
Molecular medicine reportsauthors
Yue XJ,Guo Y,Yang HJ,Feng ZW,Li T,Xu YMdoi
10.3892/mmr.2016.5411subject
Has Abstractpub_date
2016-08-01 00:00:00pages
1709-13issue
2eissn
1791-2997issn
1791-3004journal_volume
14pub_type
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