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08.02.2020 | Original Article

MicroRNA-205-5p Promotes Unstable Atherosclerotic Plaque Formation In Vivo

Cardiovascular Drugs and Therapy
Xiandong Meng, Jianjiao Yin, Xinli Yu, Yonggang Guo
Wichtige Hinweise

Electronic supplementary material

The online version of this article (https://​doi.​org/​10.​1007/​s10557-020-06935-9) contains supplementary material, which is available to authorized users.

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Atherosclerosis is a narrowing of the arteries caused by plaque buildup. MicroRNAs (miRNAs) have been proposed to participate in the pathogenesis of atherosclerosis. Here, we aimed to investigate miR-205-5p’s role in promoting atherosclerotic progression.


Knock-in (KI) mice with human/murine miR-205-5p within the murine host gene for miR-205 (MIR205HG) were crossed with apolipoprotein E knockout (Apoe−/−) mice. This miR-205KI Apoe−/− murine model was employed to study the impact of miR-205-5p in Apoe−/− mice susceptible to atherosclerotic plaque formation.


miR-205KI Apoe−/−mice developed larger, more unstable plaques relative to their Apoe−/− counterparts (0.45 vs. 0.26 mm2, P < 0.001). miR-205KI Apoe−/− mice exhibited lower serum levels of high-density lipoprotein cholesterol (HDL-C) (5.18 vs. 19.31 mg/dL, P < 0.001) and triglycerides (32.79 vs. 156.76 mg/dL, P < 0.001) with system-wide reversal of cholesterol transport. Macrophages derived from miR-205KI Apoe−/− mice exhibited ~ 20% lowered cholesterol efflux capability with enhanced pro-inflammatory gene expression through lipid raft formation. Bone marrow transplantation demonstrated that bone marrow (BM) donor cells with miR-205-5pKI simulated plaque formation independent of the recipients’ miR-205-5p status.


miR-205-5p encourages unstable atherogenesis in vivo. miR-205-5p also adversely influences lipid metabolism and promotes a pro-inflammatory macrophage phenotype. Our findings advocate miR-205-5p as a potential therapeutic target for combating unstable atherogenesis.

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