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• W2009182854 abstract "Purpose.: To evaluate the expression profile of microRNAs (miRNAs) and their roles in human Tenon's fibroblasts (HTFs), and to establish an miRNA-based gene-silencing method for antifibrosis in vitro. Methods.: The miRNA expression profile was analyzed by microarray using quiescent and transforming growth factor beta 1 (TGFβ1)–stimulated primary HTFs, respectively. Candidate miRNAs were identified by quantitative RT-PCR. miRNAs potentially targeting fibrosis-related genes were predicted using a published algorithm. Predicted fibrosis-related genes regulated by candidate miRNAs were confirmed by transfection of the miRNA into HTF culture (with or without TGFβ1 treatment), followed by quantitative RT-PCR and Western blot analysis. Results.: In all, 38 miRNAs were identified to be upregulated and 31 downregulated, in TGFβ1-stimulated HTFs. Among those, the miR-29b, downregulated in TGFβ1-treated HTFs, targeted a cadre of mRNAs that encode proteins involved in fibrosis, including PI3Kp85α, Sp1, and collagen type I alpha1 (Col1A1). Treatment of HTFs with TGFβ1 activated the PI3K/Akt/Sp1 pathway and, consequently, induced an increase in the expression of type I collagen. Overexpression of miR-29b inhibited the PI3K/Akt/Sp1 pathway, and attenuated the expression of Col1A1. Conclusions.: miR-29b acted as a suppressor of type I collagen gene by repressing the PI3K/Akt/Sp1 pathway in HTFs. Overexpression of miR-29b protected subconjunctival tissues against collagen production and fibrosis. These findings provided a novel rationale for the development of miRNA-based strategies for attenuating scar formation after glaucoma filtering surgery." @default.
• W2009182854 created "2016-06-24" @default.
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• W2009182854 creator A5056137294 @default.
• W2009182854 date "2012-03-26" @default.
• W2009182854 modified "2023-10-10" @default.
• W2009182854 title "Suppression of Type I Collagen Expression by miR-29b via PI3K, Akt, and Sp1 Pathway in Human Tenon's Fibroblasts" @default.
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• W2009182854 doi "https://doi.org/10.1167/iovs.11-8670" @default.
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