Introduction:
Hsa_circ_0054633 has been found to be elevated in the blood of coronary artery disease (CAD) patients. However, the molecular mechanism and the role of hsa_circ_0054633 in the pathogenesis of CAD have not been reported in detail.

Material and methods:
The expression of hsa_circ_0054633, microRNA (miR)-107 and thioredoxin-interacting protein (TXNIP) mRNA was measured using quantitative real-time polymerase chain reaction. Human artery vascular smooth muscle cell (HA-VSMC) proliferation, cell cycle, and migration were detected by cell counting kit-8 assay, flow cytometry and transwell assay, respectively. The generation of reactive oxygen species (ROS) was analyzed by dichlorofluorescein diacetate (DCFH-DA) assay. Western blot was utilized to determine the levels of proliferating cell nuclear antigen (PCNA), cyclin D1, matrix metallopeptidase 9 (MMP-9), Mn-superoxide dismutase (SOD2) and TXNIP protein. The interaction between miR-107 and hsa_circ_0054633 or TXNIP was confirmed by dual-luciferase reporter, RNA immunoprecipitation assay or pull-down assay.

Results:
Hsa_circ_0054633 was elevated in the plasma of CAD patients, and might be a potential blood biomarker for CAD prediction. Hsa_circ_0054633 silencing reversed PDGF-BB-induced promotion on HA-VSMC proliferation, cell cycle, migration and ROS production. MiR-107 directly interacted with hsa_circ_0054633 and TXNIP, and hsa_circ_0054633 regulated TXNIP expression by sponging miR-107. Besides, rescue assay indicated that the action of hsa_circ_0054633 silencing on PDGF-BB-treated HA-VSMCs could be attenuated by miR-107 inhibition or TXNIP overexpression, respectively.

Conclusions:
Hsa_circ_0054633 knockdown protected HA-VSMCs against PDGF-BB-induced dysfunction through regulating miR-107/TXNIP axis, suggesting a potential therapeutic target for coronary atherosclerosis.