Down-regulation of microRNA-342-5p or Up-regulation of Wnt3a Inhibits Angiogenesis and Maintains Atherosclerotic Plaque Stability in Atherosclerosis Mice

Nanoscale Research Letters

Yan Ma¹  Mingyue Zhang²  Yulu Luo²  Qinggong Wang²  Haixia Sun²  Fang Li²  Jinhua Feng³  Ding Cai⁴  Quanzhong Hu⁴ 

[1] Department of Cardiac Ultrasound, Haixi People’s Hospital;Department of Cardiac Ultrasound, Qinghai Provincial People’s Hospital;Department of General Practitioner, Qinghai Provincial People’s Hospital;Department of Neurology, Qinghai Provincial People’s Hospital;

关键词: Atherosclerosis;    MicroRNA-342-5p;    Wnt3a;    Vulnerable plaque;    Vulnerability index;    Microvessel density;   

DOI  :  10.1186/s11671-021-03608-w

来源: DOAJ

【 摘 要 】

Abstract Evidence has demonstrated that microRNA-342-5p (miR-342-5p) is implicated in atherosclerosis (AS), but little is known regarding its intrinsic regulatory mechanisms. Here, we aimed to explore the effect of miR-342-5p targeting Wnt3a on formation of vulnerable plaques and angiogenesis of AS. ApoE−/− mice were fed with high-fat feed for 16 w to replicate the AS vulnerable plaque model. miR-342-5p and Wnt3a expression in aortic tissues of AS were detected. The target relationship between miR-342-5p and Wnt3a was verified. Moreover, ApoE−/− mice were injected with miR-342-5p antagomir and overexpression-Wnt3a vector to test their functions in serum lipid levels, inflammatory and oxidative stress-related cytokines, aortic plaque stability and angiogenesis in plaque of AS mice. miR-342-5p expression was enhanced and Wnt3a expression was degraded in aortic tissues of AS mice and miR-342-5p directly targeted Wnt3a. Up-regulating Wnt3a or down-regulating miR-342-5p reduced blood lipid content, inflammatory and oxidative stress levels, the vulnerability of aortic tissue plaque and inhibited angiogenesis in aortic plaque of AS mice. Functional studies show that depleting miR-342-5p can stabilize aortic tissue plaque and reduce angiogenesis in plaque in AS mice via restoring Wnt3a.

【 授权许可】

Unknown