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