Hsa_circ_0000345 regulates the cellular development of ASMCs in response to oxygenized low-density lipoprotein.

Abstract

The interaction between circRNAs and atherosclerosis has been extensively studied. However, more novel circRNAs need to be explored to help establish a perfect regulatory network. In the present research, hsa_circ_0000345 was demonstrated to regulate cellular development of oxygenized low‐density lipoprotein (ox‐LDL)‐treated aortic smooth muscle cells (ASMCs), which was closely related to the occurrence and progress of atherosclerosis. Ox‐LDL exposure remarkably decreased hsa_circ_0000345 expression in ASMCs. Transfection‐induced hsa_circ_0000345 overexpression activated cell viability (detected by an MTT assay) and restrained cellular apoptosis (analysed by flow cytometry) in the atherosclerosis cellular model. While down‐regulation of hsa_circ_0000345 reduced cell viability and promoted cell apoptosis. In addition, the data of the cell cycle distribution analysis and trans‐well assay indicated that cell cycle progression was arrested at the G1 phase while cell invasion was enhanced in ASMCs following treatment of ox‐LDL in the context of hsa_circ_0000345 OE plasmids. In addition, up‐regulation of hsa_circ_0000345 supported HIF‐1α at both the mRNA and protein level, and down‐regulation of hsa_circ_0000345 reduced HIF‐1α expression. Overall, the above findings revealed that hsa_circ_0000345 was a dramatic regulator of ASMCs proliferation, apoptosis and invasion in response to ox‐LDL treatment. Hsa_circ_0000345 was identified as a protector of cell viability during ox‐LDL induced cell development.