Atherosclerosis (AS) is the main reason for most
cardiovascular diseases.
Circular RNA hsa_circ_0044073 (circ_0044073) has been found to promote AS progression. However, the specific regulatory mechanism of circ_0044073 in AS progression remains unclear.In this study,
oxidized low-density lipoprotein (
Ox-LDL) -stimulated human vascular smooth muscle cells (VSMCs) were used as AS cell models. The expression changes of circ_0044073 in serum samples and
Ox-LDL-stimulated human VSMCs were assessed via real-time quantitative polymerase chain reaction (RT-qPCR). Cell viability, proliferation, colony formation, migration, and invasion were assessed using 3- (4,5-Dimethylthiazol-2-yl) -2,5-Diphenyltetrazolium
Bromide (MTT),
5-ethynyl-2'-deoxyuridine (EDU), colony formation, and transwell assays. Some
protein levels were detected via Western blotting. The regulatory mechanism of circ_0044073 was predicted using bioinformatics analysis and validated by dual-
luciferase reporter and
RNA pull-down assays.We observed an overt increase in circ_0044073 expression in serum samples derived from AS patients and
Ox-LDL-stimulated human VSMCs. Circ_0044073 was identified as a miR-377-3p sponge. Either circ_0044073 knockdown or miR-377-3p overexpression could impair
Ox-LDL-induced human VSMC proliferation, migration, invasion, and
inflammation.
AURKA served as a miR-377-3p target, and circ_0044073 regulated
AURKA expression by adsorbing miR-377-3p. Furthermore,
AURKA overexpression partly reversed the effects of circ_0044073 inhibition on
Ox-LDL-induced human VSMC proliferation, migration, invasion, and
inflammation.Circ_0044073 promoted AS progression by elevating
AURKA expression by functioning as a miR-377-3p sponge. Providing a proof-of-concept demonstration to support circ_0044073 might be a target for AS treatment.