ArticleOpen medicine (Warsaw, Poland)2023
Knockdown of circ_0113656 assuages oxidized low-density lipoprotein-induced vascular smooth muscle cell injury through the miR-188-3p/IGF2 pathway.
Article in Open medicine (Warsaw, Poland), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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5 authors at 2 institutions in 1 country.
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Abstract
Circular RNA (circRNA) is involved in the pathogenesis of atherosclerosis (AS). The present work analyzed the RNA expression of circ_0113656, microRNA-188-3p (miR-188-3p), and insulin-like growth factor 2 (IGF2) by quantitative real-time polymerase chain reaction. The protein expression of proliferating cell nuclear antigen (PCNA), matrix metalloprotein 2 (MMP2), and IGF2 was detected by Western blotting. Cell viability, proliferation, invasion, and migration were analyzed using the cell counting kit-8, 5-ethynyl-2'-deoxyuridine, transwell invasion, and wound-healing assays, respectively. The interactions among circ_0113656, miR-188-3p, and IGF2 were identified by dual-luciferase reporter assay and RNA immunoprecipitation assay. The results showed that circ_0113656 and IGF2 expression were significantly upregulated, while miR-188-3p was downregulated in the blood of AS patients and oxidized low-density lipoprotein (ox-LDL)-treated HVSMCs in comparison with controls. The ox-LDL treatment induced HVSMC proliferation, migration, and invasion accompanied by increases in PCNA and MMP2 expression; however, these effects were attenuated after circ_0113656 knockdown. Circ_0113656 acted as a miR-188-3p sponge and it regulated ox-LDL-induced HVSMC disorders by binding to miR-188-3p. Besides, the regulation of miR-188-3p in ox-LDL-induced HVSMC injury involved IGF2. Further, the depletion of circ_0113656 inhibited IGF2 expression by interacting with miR-188-3p. Thus, the circ_0113656/miR-188-3p/IGF2 axis may mediate ox-LDL-induced HVSMC disorders in AS, providing a new therapeutic strategy for AS.
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