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• W2048496654 abstract "The activation of hepatic stellate cells (HSCs) is the key event of the pathogenesis of hepatic fibrosis. Platelet-derived growth factor (PDGF) is the most potent mitogen for HSCs, and PDGF receptor-β subunit (PDGFR-β) is required for the proliferation of HSCs induced by PDGF. In this study, a high gene-silencing-efficacy PDGFR-β small interference RNA (siRNA) was synthesized that could suppress the PDGFR-β expression and inhibit the activation and proliferation but could not induce the apoptosis of HSCs in vitro. To avoid the side effect of nonspecific interference of PDGFR-β, we constructed an HSCs-specific short hairpin RNA (shRNA) expression plasmid in which PDGFR-β shRNA was driven by a glial fibrillary acidic protein (GFAP) promoter. The double-staining immunofluorescence examination indicated that GFAP promoter could target the transgene expression into HSCs in carbon tetrachloride induced acute injured rat's liver and bile duct ligation (BDL)-induced chronic injured rat's liver. Furthermore, HSCs-specific PDGFR-β shRNA could relieve liver injury and hepatic fibrosis in the rat's model induced by BDL. This study demonstrates that PDGFR-β siRNA may be presented as an antifibrogenic agent. The application of HSCs-specific RNA interference induced by the GFAP promoter might supply a new powerful tool for cell-specific gene therapy of hepatic fibrogenesis." @default.
• W2048496654 created "2016-06-24" @default.
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• W2048496654 date "2008-05-29" @default.
• W2048496654 modified "2023-09-23" @default.
• W2048496654 title "Targeted inhibition of platelet-derived growth factor receptor-β subunit in hepatic stellate cells ameliorates hepatic fibrosis in rats" @default.
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• W2048496654 doi "https://doi.org/10.1038/gt.2008.93" @default.
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