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MiR-21 Participates in Anti-VEGF-Induced Epithelial Mesenchymal Transformation in RPE Cells
Xianghui Hao1, Yingbin Hua1, Chaohui Xie1
1State Key Laboratory Cultivation Base, Shandong Provincial Key Laboratory of Ophthalmology, Shandong Eye Institute, Shandong First Medical University & Shandong Academy of Medical Sciences, Qingdao, People's Republic of China.
Background:
To explore the role and possible mechanism of miR-21 in anti-VEGF drug-induced epithelial-mesenchymal transformation (EMT) in human retinal pigment epithelium (ARPE-19) cells, and to seek more therapeutic targets to improve prognosis vision.
Methods:
ARPE-19 cells were exposed to clinical dosage of bevacizumab and miR-21 expression was measured by real-time polymerase chain reaction (RT-PCR) assay. MiR-21 mimic and inhibitor were transfected into bevacizumab-induced ARPE-19, the expression of α-smooth muscle actin (α-SMA), E-cadherin, and SNAI1 were detected by cell immunofluorescence and Western blotting.
Results:
Clinical dosage of bevacizumab caused EMT and enhanced miR-21 expression in ARPE-19 cells (P<0.05). The inhibition of miR-21 attenuated the EMT effect of bevacizumab, while overexpression of miR-21 promoted this activity (P<0.05). The SNAI1 was up-regulated by bevacizumab and promotion was partially suppressed by the miR-21 inhibitor and aggravated by the miR-21 mimic (P<0.05).
Conclusion:
MiR-21 promotes bevacizumab-induced EMT in ARPE cells which is significantly positively correlated with SNAI1. MiR-21 might be a potential miRNA-based therapeutic target for reducing bevacizumab-induced subretinal fibrosis.
Insights
MicroRNA-21 (miR-21) promotes anti-VEGF drug-induced epithelial-mesenchymal transition (EMT) in retinal cells. Inhibiting miR-21 may reduce bevacizumab-induced fibrosis, offering a potential therapeutic target.
Area of Science:
- Ophthalmology
- Molecular Biology
- Cell Biology
Background:
- Anti-VEGF therapies like bevacizumab can induce epithelial-mesenchymal transition (EMT) in retinal pigment epithelium (ARPE-19) cells.
- The role of microRNA-21 (miR-21) in this process and its potential as a therapeutic target remain to be fully elucidated.
Purpose of the Study:
- To investigate the role and mechanism of miR-21 in bevacizumab-induced EMT in ARPE-19 cells.
- To identify potential therapeutic targets for improving visual prognosis by modulating miR-21.
Main Methods:
- ARPE-19 cells were treated with bevacizumab, and miR-21 expression was quantified using RT-PCR.
- miR-21 mimic and inhibitor transfections were performed to assess effects on EMT markers (α-SMA, E-cadherin, SNAI1) via immunofluorescence and Western blotting.
Main Results:
- Bevacizumab treatment induced EMT and increased miR-21 expression in ARPE-19 cells (P<0.05).
- miR-21 inhibition attenuated bevacizumab-induced EMT, while miR-21 overexpression promoted it (P<0.05).
- Bevacizumab upregulated SNAI1, an effect partially suppressed by miR-21 inhibition and aggravated by miR-21 mimic (P<0.05).
Conclusions:
- miR-21 promotes bevacizumab-induced EMT in ARPE cells, correlating positively with SNAI1 expression.
- miR-21 represents a potential miRNA-based therapeutic target for mitigating bevacizumab-induced subretinal fibrosis.
