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Hypoxia induces the activation of human hepatic stellate cells LX‐2 through TGF‐β signaling pathway
Author(s) -
Shi Yue-Feng,
Fong Chi-Chun,
Zhang Qi,
Cheung Pik-Yuen,
Tzang Chi-Hung,
Wu Rudolf S.S.,
Yang Mengsu
Publication year - 2007
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2006.12.010
Subject(s) - hepatic stellate cell , smad , hypoxia (environmental) , signal transduction , blot , microbiology and biotechnology , phosphorylation , gene expression , chemistry , biology , transforming growth factor , medicine , endocrinology , gene , biochemistry , oxygen , organic chemistry
Hypoxia is a common environmental stress factor and is also associated with various physiological and pathological conditions such as fibrogenesis. The activation of hepatic stellate cells (HSCs) is the key event in the liver fibrogenesis. In this study, the behavior of human HSCs LX‐2 in low oxygen tension (1% O 2 ) was analyzed. Upon hypoxia, the expression of HIF‐1α and VEGF gene was induced. The result of Western blotting showed that the expression of α‐SMA was increased by hypoxic stimulation. Furthermore, the expression of MMP‐2 and TIMP‐1 genes was increased. Hypoxia also elevated the protein expression of the collagen type I in LX‐2 cells. The analysis of TGF‐β/Smad signaling pathway showed that hypoxia potentiated the expression of TGF‐β1 and the phosphorylation status of Smad2. Gene expression profiles of LX‐2 cells induced by hypoxia were obtained by using cDNA microarray technique.