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  • Title: MicroRNA-184 is a key molecule responsible for the transforming growth factor-β2 -induced epithelial-mesenchymal transition in human lens epithelial-B3 cells.
    Author: Chen Y, Fan D, Zhang X, Han S, Wei X, Wang Y, Song L.
    Journal: Clin Exp Ophthalmol; 2020 Aug; 48(6):821-829. PubMed ID: 32356563.
    Abstract:
    BACKGROUND: TGF-β2-induced epithelial-mesenchymal transition (EMT) is an important mechanism for posterior capsule opacity (PCO) in lens epithelial cells (LECs). This study aimed to investigate if MicroRNA-184 (miR-184) plays a role in the TGF-β2-induced EMT in LECs. METHODS: Human LECs (HLE-B3 cells) were used in this study. Quantitative real-time polymerase chain reaction (PCR) (qRT-PCR) was performed to analyse miR-184 expressions in HLE-B3 treated with TGF-β2 at different concentrations (0-15 ng/mL) and different time (10 ng/mL, 0-48 hours). After transfection of miR-184 mimics or miR-184 inhibitor, cells were treated with 10 ng/mL TGF-β2 for 24 hours, and the expression levels of miR-184, E-cadherin, vimentin, zinc finger E-box binding homeobox 2 (ZEB2), α-Smooth muscle actin (α-SMA), Collagen 1 and bin3 were determined by qRT-PCR and Western blot, respectively. RESULTS: TGF-β2 treatment significantly downregulated E-cadherin and upregulated vimentin generally in a dose-dependent and time-dependent manner. TGF-β2 treatment significantly elevated the level of miR-184 in both dose- and time-dependent manners. In addition, transfection of miR-184 inhibitor RNA significantly attenuated TGF-β2-induced downregulation of E-cadherin as well as upregulation of vimentin, ZEB2, α-SMA and Collagen 1, whereas transfection of miR-184 mimic further enhanced the effects of TGF-β2 on the expressions of these markers. Furthermore, TGF-β2 treatment significantly downregulated bin3, and transfection of miR-184 mimic and miR-184 inhibitor significantly enhanced and attenuated the inhibition effect of TGF-β2 on bin3, respectively. CONCLUSIONS: miR-184 plays a key role in the TGF-β2-induced EMT in LECs, and bin3 may be a downstream protein.
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