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miR-454-3p prevents ox-LDL-induced apoptosis in HAECs by targeting TRPC3
Luming Liao1,2, Qiaolan Yang3, Hailiang Li3
1The Second School of Clinical Medicine, Southern Medical University, Guangzhou, Guangdong 510280, P.R. China.
Abstract:
Endothelial-cell (EC) apoptosis serves a vital role in the pathogenesis of atherosclerosis. Accumulating evidence has implicated microRNA (miRNA/miR) dysregulation in EC apoptosis. Although the role of miR-454-3p in carcinogenesis has been well documented, its role and underlying mechanism in EC apoptosis remain unclear. In the present study, the results revealed that miR-454-3p expression was substantially downregulated in human aortic endothelial cells (HAECs) following oxidized low-density lipoprotein (ox-LDL) treatment. miR-454-3p suppression significantly attenuated the viability of HAECs, while miR-454-3p overexpression repressed ox-LDL-induced HAEC apoptosis. Bioinformatics analysis and luciferase reporter assays revealed that transient receptor potential canonical 3 (TRPC3), a key regulator of atherosclerosis development, was the direct target of miR-454-3p. Furthermore, TRPC3 overexpression abolished the anti-apoptotic effect of miR-454-3p on HAECs. These results revealed a novel role of miR-454-3p in ox-LDL-induced apoptosis in HAECs.
Insights
MicroRNA-454-3p (miR-454-3p) protects endothelial cells from apoptosis induced by oxidized low-density lipoprotein (ox-LDL). This study identifies miR-454-3p as a key regulator in atherosclerosis pathogenesis.
Area of Science:
- Molecular Biology
- Cardiovascular Research
- Cell Biology
Background:
- Endothelial-cell (EC) apoptosis is crucial in atherosclerosis development.
- MicroRNA (miRNA) dysregulation is implicated in EC apoptosis.
- The specific role of miR-454-3p in EC apoptosis is not well understood.
Purpose of the Study:
- To investigate the role and mechanism of miR-454-3p in oxidized low-density lipoprotein (ox-LDL)-induced human aortic endothelial cell (HAEC) apoptosis.
- To identify the direct target of miR-454-3p involved in EC apoptosis.
Main Methods:
- Human aortic endothelial cells (HAECs) were treated with ox-LDL.
- miR-454-3p expression levels were measured.
- Cell viability and apoptosis assays were performed.
- Bioinformatics analysis and luciferase reporter assays were used to identify miR-454-3p targets.
- TRPC3 expression was manipulated to assess its interaction with miR-454-3p.
Main Results:
- miR-454-3p expression was significantly downregulated in HAECs treated with ox-LDL.
- Suppression of miR-454-3p reduced HAEC viability and promoted apoptosis.
- Overexpression of miR-454-3p inhibited ox-LDL-induced HAEC apoptosis.
- Transient receptor potential canonical 3 (TRPC3) was identified as a direct target of miR-454-3p.
- TRPC3 overexpression reversed the anti-apoptotic effects of miR-454-3p.
Conclusions:
- miR-454-3p plays a protective role against ox-LDL-induced apoptosis in HAECs.
- The miR-454-3p/TRPC3 axis is a novel mechanism regulating EC apoptosis in atherosclerosis.
- miR-454-3p may represent a potential therapeutic target for atherosclerosis.
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