Basic & Clinical Medicine ›› 2025, Vol. 45 ›› Issue (4): 486-492.doi: 10.16352/j.issn.1001-6325.2025.04.0486

• Original Articles • Previous Articles     Next Articles

Upregulation of miR-152 inhibits proliferation and migration of human vascular smooth muscle cells induced by ox-LDL

ZHOU Jing, QU Miao*   

  1. Function Department, Baoji Central Hospital, Baoji 721008, China
  • Received:2024-07-31 Revised:2024-12-25 Online:2025-04-05 Published:2025-03-24

Abstract: Objective To investigate the roles of miR-152 and Rho-associated coiled-coil kinase 1 (ROCK1) in vascular smooth muscle cells (VSMCs) treated with oxidized low-density lipoprotein (ox-LDL). Methods Human vascular smooth muscle cells CRL-1999 were intervened with ox-LDL to establish an in vitro atherosclerosis model. miR-152 mimic and ROCK1 siRNA were transfected into corresponding cells. RT-qPCR was used to detect the expression of miR-152 and ROCK1 mRNA. The CCK-8 method was used to assess cell proliferation activity, and the Transwell assay was used to test cell migration ability. A luciferase reporter gene assay was conducted to determine the targeting relationship between miR-152 and ROCK1. Results CRL-1999 cells treated with 100 μg/mL ox-LDL for 48 hours showed the maximum proliferation rate. Compared with the untreated control group, the relative expression of miR-152 in the ox-LDL-induced group was significantly decreased (P<0.05). Transfection of miR-152 mimic significantly reduced the proliferation and migration of CRL-1999 cells (P<0.05). The luciferase reporter gene assay indicated that miR-152 targets ROCK1, and expression of ROCK1 mRNA and protein in miR-152 mimic group was reduced(P<0.05). Transfection of ROCK1 siRNA also significantly decreased the proliferation and migration of CRL-1999 cells(P<0.05). Conclusions miR-152 inhibits the ox-LDL induced proliferation and migration of CRL-1999 cells by downregulating ROCK1 expression, which may be a potential therapeutic target for atherosclerosis.

Key words: miR-152, atherosclerosis, Rho-associated coiled-coil kinase 1, vascular smooth muscle, proliferation, migration

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