Noncoding RNAs in vascular inflammation and atherosclerosis

Cochain, Clément; Zernecke, Alma

doi:10.1097/mol.0000000000000108

Cited by 6 publications

(2 citation statements)

References 53 publications

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“…The important role of miRNAs in cardiovascular diseases, including atherosclerosis, has been evidenced by recent observations 7–9,26–28 . MiR-33a/b, miR-19b, miR-144-3p, miR-92a, miR-155, miR-145/143, and miR-342-5p have been identified to promote atherosclerosis development 10–12,15–20,29–31 .…”

Section: Discussionmentioning

confidence: 98%

MicroRNA-181a-5p and microRNA-181a-3p cooperatively restrict vascular inflammation and atherosclerosis

Yuan²,

Zhang³

et al. 2019

Cell Death Dis

108

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MicroRNAs have emerged as important post-transcriptional regulators of gene expression and are involved in diverse diseases and cellular process. Decreased expression of miR-181a has been observed in the patients with coronary artery disease, but its function and mechanism in atherogenesis is not clear. This study was designed to determine the roles of miR-181a-5p, as well as its passenger strand, miR-181a-3p, in vascular inflammation and atherogenesis. We found that the levels of both miR-181a-5p and miR-181a-3p are decreased in the aorta plaque and plasma of apoE −/− mice in response to hyperlipidemia and in the plasma of patients with coronary artery disease. Rescue of miR-181a-5p and miR-181a-3p significantly retards atherosclerotic plaque formation in apoE −/− mice. MiR-181a-5p and miR-181a-3p have no effect on lipid metabolism but decrease proinflammatory gene expression and the infiltration of macrophage, leukocyte and T cell into the lesions. In addition, gain-of-function and loss-of-function experiments show that miR-181a-5p and miR-181a-3p inhibit adhesion molecule expression in HUVECs and monocytes-endothelial cell interaction. MiR-181a-5p and miR-181a-3p cooperatively receded endothelium inflammation compared with single miRNA strand. Mechanistically, miR-181a-5p and miR-181a-3p prevent endothelial cell activation through blockade of NF-κB signaling pathway by targeting TAB2 and NEMO, respectively. In conclusion, these findings suggest that miR-181a-5p and miR-181a-3p are both antiatherogenic miRNAs. MiR-181a-5p and miR-181a-3p mimetics retard atherosclerosis progression through blocking NF-κB activation and vascular inflammation by targeting TAB2 and NEMO, respectively. Therefore, restoration of miR-181a-5p and miR-181a-3p may represent a novel therapeutic approach to manage atherosclerosis.

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Section: Discussionmentioning

confidence: 98%

MicroRNA-181a-5p and microRNA-181a-3p cooperatively restrict vascular inflammation and atherosclerosis

Yuan²,

Zhang³

et al. 2019

Cell Death Dis

108

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“…suppressors of cytokine signaling—SOCS) [2] , [3] , [11] . Noncoding RNA, particularly microRNA (miRNA), are emerging as future potential targets in dampening cytokine-mediated inflammation in atherosclerosis [248] . For example, deficiency of mIR155, whose expression is stimulated by miR-342-5p [249] , reduces inflammatory responses in mouse model systems [250] .…”

Section: Conclusion and Therapeutic Perspectivesmentioning

confidence: 99%

Cytokines in atherosclerosis: Key players in all stages of disease and promising therapeutic targets

Ramji

Davies

2015

Cytokine & Growth Factor Reviews

402

371

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Atherosclerosis, a chronic inflammatory disorder of the arteries, is responsible for most deaths in westernized societies with numbers increasing at a marked rate in developing countries. The disease is initiated by the activation of the endothelium by various risk factors leading to chemokine-mediated recruitment of immune cells. The uptake of modified lipoproteins by macrophages along with defective cholesterol efflux gives rise to foam cells associated with the fatty streak in the early phase of the disease. As the disease progresses, complex fibrotic plaques are produced as a result of lysis of foam cells, migration and proliferation of vascular smooth muscle cells and continued inflammatory response. Such plaques are stabilized by the extracellular matrix produced by smooth muscle cells and destabilized by matrix metalloproteinase from macrophages. Rupture of unstable plaques and subsequent thrombosis leads to clinical complications such as myocardial infarction. Cytokines are involved in all stages of atherosclerosis and have a profound influence on the pathogenesis of this disease. This review will describe our current understanding of the roles of different cytokines in atherosclerosis together with therapeutic approaches aimed at manipulating their actions.

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Systematically analyses of the common dysregulated networks to understand the common pathologies between T2D and atherosclerosis

Lin

Yang

Sun

et al. 2018

Gene

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Noncoding RNAs in vascular inflammation and atherosclerosis

Cited by 6 publications

References 53 publications

MicroRNA-181a-5p and microRNA-181a-3p cooperatively restrict vascular inflammation and atherosclerosis

MicroRNA-181a-5p and microRNA-181a-3p cooperatively restrict vascular inflammation and atherosclerosis

Cytokines in atherosclerosis: Key players in all stages of disease and promising therapeutic targets

Systematically analyses of the common dysregulated networks to understand the common pathologies between T2D and atherosclerosis

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