Affiliation:
1. Jinan University
2. the Second Affiliated Hospital of Bengbu Medical College
3. the First Affiliated Hospital of Bengbu Medical College
4. HuaiBei General Miner Hospital
Abstract
Abstract
Atherosclerosis is one of the main causes of cardiovascular diseases. Aquaporin 9 (AQP9), a triglyceride channel is permeable to water, monocarboxylic acids, glycerol and lactic acid. However, the role of AQP9 in atherosclerosis is not clear. In present study, we predicted that miR-330-3p might regulate AQP9 in atherosclerosis through bioinformatics analysis, then we established atherosclerosis model by ApoE −/− mouse (C57BL/6) with high fat diet (HFD). Hematoxylin and eosin (H&E) and Oil red O were used to stain atherosclerotic lesions. Furthermore, we used 100 µg/mL ox-LDL treat human umbilical vein endothelial cells (HUVECs) to investigate the role of miR-330-3p and AQP9. CCK8 and EDU assays were used to investigate the cell proliferation. Wound scratch healing and transwell assays were used to measure the cells invade and migrate ability. Flow cytometry assay was used to detect apoptosis and cell cycle changes. A dual-luciferase reporter assay was performed to determine the binding of miR-330-3p and AQP9. We identified that the expression of miR-330-3p in AS mice model decreased while the expression of AQP9 increased. MiR-330-3p overexpression or down-regulation of AQP9 could reduce cell apoptosis and promote cell proliferation and migration after ox-LDL treatment. Dual-luciferase reporter assay result presented that AQP9 is directly inhibited by miR-330-3p. These results suggest that miR-330-3p inhibits atherosclerosis by regulating AQP9. Our results indicates that miR-330-3p inhibits atherosclerosis by regulating AQP9. Mir-330-3p/AQP9 axis maybe a new therapeutic target for atherosclerosis.
Publisher
Research Square Platform LLC