AI Article Synopsis
- - LINC01592 expression increases in human retinal pigment epithelial (RPE) cells when treated with TGF-β1, indicating its role in the transformation of these cells to a mesenchymal state.
- - Knockdown of LINC01592 leads to decreased levels of E-cadherin and increased levels of α-SMA and Snail, suggesting it plays a crucial role in promoting epithelial-mesenchymal transition (EMT) in RPE cells induced by TGF-β1.
- - Enhancing LINC01592 expression boosts cell viability, proliferation, and migration in response to TGF-β1, implicating it as a potential target for treating proliferative vitreoretinopathy by modulating
Article Abstract
Regulation of long-chain non-coding RNA01592 (LINC01592) in the process of transforming retinal pigment epithelial (RPE) cells into mesenchymal cells following induction by transforming growth factor beat 1 (TGF-β1) was investigated by interfering with LINC01592 expression in human RPE (hRPE) cells. LINC01592 expression in hRPE cells was significantly increased following treatment with 10 ng/mL TGF-β1 for 48 h. Expression of E-cadherin and Snail were decreased in hRPE cells following induction with TGF-β1 compared with the control group ( 0.05). Following induction by TGF-β1, expression of E-cadherin, alpha-smooth muscle actin (α-SMA), and Snail were significantly lower in the LINC01592-knockdown group compared with the negative control group ( 0.05). LINC01592 overexpression significantly enhanced the viability, proliferation, and migration of hRPE cells induced by TGF-β1 ( 0.05). Following induction by TGF-β1, E-cadherin expression was significantly decreased and α-SMA and Snail expression were significantly increased in the LINC01592-overexpression group compared with the negative control group ( 0.05). RPE cells induced by TGF-β1 exhibited epithelial-mesenchymal transition (EMT). Inhibiting LINC01592 expression could significantly reduce TGF-β1-induced EMT of hRPE cells. The regulatory effect of LINC01592 on EMT in hRPE cells induced by TGF-β1 provides a novel treatment for proliferative vitreoretinopathy.
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|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8202905 | PMC |
| http://dx.doi.org/10.18632/aging.203023 | DOI Listing |
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