In:
Clinical & Experimental Ophthalmology, Wiley, Vol. 48, No. 6 ( 2020-08), p. 821-829
Abstract:
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.
Type of Medium:
Online Resource
ISSN:
1442-6404
,
1442-9071
Language:
English
Publisher:
Wiley
Publication Date:
2020
detail.hit.zdb_id:
2094910-8
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