M-Y Wei1, R-R Lv, Z Teng. 1. Cardiovascular Department, Cangzhou Central Hospital, Cangzhou, Hebei Province, China. tengrbvvh139@163.com.
Abstract
OBJECTIVE: The aim of the study was to explore the role and mechanism of circHIPK3 in atherosclerosis. MATERIALS AND METHODS: AS model was constructed in vivo and in vitro for high fat-fed and ox-LDL treatment. RT-PCR was used to assess the level of circHIPK3. The autophagy level of HUVECs was detected by Western blot, transmission electron microscopy, and LC3II fluorescence intensity. HUVECs lipid accumulation was assessed by oil red staining. Luciferase assay was performed to verify the relationship of circRNA and miRNA, miRNA, and target gene. RESULTS: The expression of circHIPK3 was downregulated in HFD mice, and ox-LDL treated HUVECs. The level of autophagy was decreased in AS, which was reversed by overexpression of circHIPK3. Meanwhile, forced expression of circHIPK3 would reduce the accumulation of lipid in HUVECs. CONCLUSIONS: CircHIPK3 could inhibit lipid content in ox-LD-treated HUVECs via activating autophagy. This progression mechanism may target the miR-190b/ATG7 signal pathway, which indicates a suitable role in the pathogenesis of atherosclerosis.
OBJECTIVE: The aim of the study was to explore the role and mechanism of circHIPK3 in atherosclerosis. MATERIALS AND METHODS:AS model was constructed in vivo and in vitro for high fat-fed and ox-LDL treatment. RT-PCR was used to assess the level of circHIPK3. The autophagy level of HUVECs was detected by Western blot, transmission electron microscopy, and LC3II fluorescence intensity. HUVECs lipid accumulation was assessed by oil red staining. Luciferase assay was performed to verify the relationship of circRNA and miRNA, miRNA, and target gene. RESULTS: The expression of circHIPK3 was downregulated in HFD mice, and ox-LDL treated HUVECs. The level of autophagy was decreased in AS, which was reversed by overexpression of circHIPK3. Meanwhile, forced expression of circHIPK3 would reduce the accumulation of lipid in HUVECs. CONCLUSIONS:CircHIPK3 could inhibit lipid content in ox-LD-treated HUVECs via activating autophagy. This progression mechanism may target the miR-190b/ATG7 signal pathway, which indicates a suitable role in the pathogenesis of atherosclerosis.