PURPOSE: To investigate the influence of rosiglitazone on activation of human Tenon's fibroblasts (HTFs) and to access the possible mechanism. METHODS: Cultured human Tenon's fibroblasts were pretreated in two different concentrations of rosiglitazone (5 μmol/l and 10 μmol/l) before being stimulated with 5 ng/ml transforming growth factor β1 (TGF-β1). The viability and proliferation of cells were accessed by cell count kit-8 assay; Cell migration was examined by the wound closure assay; Alpha smooth muscle actin (α-SMA), connective tissue growth factor (CTGF) and type I collagen (COL I) transcription were detected by RT-qPCR; The expression and localization of α-SMA protein were examined by Western-blot analysis and Immunofluorescence staining; Western-blot analysis was also used to check the expression of CTGF, COL I peroxisome proliferator-activated receptor gamma (PPAR-γ), and phosphorylation of the signaling protein Smad2/3 RESULTS: Rosiglitazone is able to attenuate the up-regulation of α-SMA, CTGF, and COL I transcription, as well as affect protein expression, proliferation, and migration of cells; rosiglitazone also can increase PPAR-γ expression and attenuate Smad2/3 phosphorylation. CONCLUSIONS: Rosiglitazone can effectively attenuate activation of HTFs induced by TGF-β1 without obvious toxicity. The possible mechanism might be that rosiglitazone interferes with TGF-β/Smad signaling pathway.
PURPOSE: To investigate the influence of rosiglitazone on activation of human Tenon's fibroblasts (HTFs) and to access the possible mechanism. METHODS: Cultured human Tenon's fibroblasts were pretreated in two different concentrations of rosiglitazone (5 μmol/l and 10 μmol/l) before being stimulated with 5 ng/ml transforming growth factor β1 (TGF-β1). The viability and proliferation of cells were accessed by cell count kit-8 assay; Cell migration was examined by the wound closure assay; Alpha smooth muscle actin (α-SMA), connective tissue growth factor (CTGF) and type I collagen (COL I) transcription were detected by RT-qPCR; The expression and localization of α-SMA protein were examined by Western-blot analysis and Immunofluorescence staining; Western-blot analysis was also used to check the expression of CTGF, COL I peroxisome proliferator-activated receptor gamma (PPAR-γ), and phosphorylation of the signaling protein Smad2/3 RESULTS:Rosiglitazone is able to attenuate the up-regulation of α-SMA, CTGF, and COL I transcription, as well as affect protein expression, proliferation, and migration of cells; rosiglitazone also can increase PPAR-γ expression and attenuate Smad2/3 phosphorylation. CONCLUSIONS:Rosiglitazone can effectively attenuate activation of HTFs induced by TGF-β1 without obvious toxicity. The possible mechanism might be that rosiglitazone interferes with TGF-β/Smad signaling pathway.
Authors: Jun Yu; Sui Zhang; Eagle S H Chu; Minnie Y Y Go; Rebecca H Y Lau; Junhong Zhao; Chung-Wah Wu; Lixin Tong; Jingmin Zhao; Terence C W Poon; Joseph J Y Sung Journal: Int J Biochem Cell Biol Date: 2010-02-13 Impact factor: 5.085
Authors: Hiroshi Nakamura; Shahid S Siddiqui; Xiang Shen; Asrar B Malik; Jose S Pulido; Nalin M Kumar; Beatrice Y J T Yue Journal: Mol Vis Date: 2004-10-04 Impact factor: 2.367
Authors: M F Cordeiro; A Mead; R R Ali; R A Alexander; S Murray; C Chen; C York-Defalco; N M Dean; G S Schultz; P T Khaw Journal: Gene Ther Date: 2003-01 Impact factor: 5.250