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  • Title: Rosiglitazone attenuates activation of human Tenon's fibroblasts induced by transforming growth factor-β1.
    Author: Fan F, Li Y, Duan X, Zhao T, Pan D, Chen H.
    Journal: Graefes Arch Clin Exp Ophthalmol; 2012 Aug; 250(8):1213-20. PubMed ID: 22215258.
    Abstract:
    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.
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