Anzeige
Erschienen in:
27.01.2022 | Original Article
CircCHMP5 Contributes to Ox-LDL-induced Endothelial Cell Injury Through the Regulation of MiR-532-5p/ROCK2 axis
Erschienen in: Cardiovascular Drugs and Therapy | Ausgabe 6/2023
Einloggen, um Zugang zu erhaltenAbstract
Background
Aberrant expression of circular RNA (circRNA) has been demonstrated to be related to atherosclerosis (AS) formation. However, the mechanism of circCHMP5 (also known as hsa_circ_0003575) in AS formation remains unclear.
Methods
Oxidized low-density lipoprotein (ox-LDL) was used to treat human umbilical vein endothelial cells (HUVECs) to construct a cell injury model. The expression level of circCHMP5, miR-532-5p, and Rho-associated protein kinase 2 (ROCK2) was measured using quantitative real-time PCR. Cell cycle, apoptosis, proliferation, and angiogenesis were determined by flow cytometry, 5-ethynyl-2′-deoxyuridine (EdU) assay, and tube formation assay. In addition, the protein expression of apoptosis markers, inflammation factors, and ROCK2 was detected by western blot analysis. The interaction between miR-532-5p and circCHMP5 or ROCK2 was assessed by dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay.
Results
Our results indicated that circCHMP5 was overexpressed in ox-LDL-induced HUVECs. CircCHMP5 knockdown promoted cell cycle, proliferation, and angiogenesis while inhibiting apoptosis and inflammation in ox-LDL-induced HUVECs. MiR-532-5p could be sponged by circCHMP5, and its inhibitor reversed the negative regulation of si-circCHMP5 on ox-LDL-induced HUVECs injury. ROCK2, a target of miR-532-5p, reversed the inhibition effect of miR-532-5p on ox-LDL-induced HUVECs injury. Furthermore, we confirmed that circCHMP5 upregulated ROCK2 by sponging miR-532-5p.
Conclusion
To sum up, our data showed that circCHMP5 regulated the miR-532-5p/ROCK2 axis to accelerate ox-LDL-induced HUVECs injury, confirming that circCHMP5 might be a potential target for AS treatment.
