OxLDL up‐regulates microRNA‐29b, leading to epigenetic modifications of
            <i>MMP‐2/MMP‐9</i>
            genes: a novel mechanism for cardiovascular diseases

Chen, Ku Chung; Wang, Yung Song; Hu, Ching Yu; Chang, Wei Chiao; Liao, Yi‐Chu; Dai, Chia Yen; Juo, Suh Hang Hank

doi:10.1096/fj.10-174904

Cited by 203 publications

(133 citation statements)

References 48 publications

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“…Various miRNAs have effects on controlling the integrity of vessels and the function of macrophage in every stage of atherosclerosis. The work from Chen's group suggested that miR-29b was up-regulated in vascular smooth muscle cells (VSMCs) with ox-LDL treatment, which might target on MMP2 leading to a reduction of VSMC migration [13]. Lovren and colleagues have shown that overexpressing miR-145 in VSMCs decreased the plaque size of atherosclerosis and favor plaque stability [14].…”

Section: Big Nucleusmentioning

confidence: 99%

MicroRNA Let-7g and Atherosclerosis Plaque Stabilization

Yin¹,

Zhang²,

Hou³

et al. 2017

WJCD

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Vascular atherosclerotic vulnerable plaque rupture is the primary cause of acute myocardial infarctions and strokes. Thus, stabilization of vulnerable plaques is of important clinical endeavor to decrease the fatal risk of atherosclerosis. Inflammatory infiltration, apoptosis of endothelial cells (ECs) and vascular smooth muscle cells (VSMCs), destruction of extracellular matrix (ECM) or collagen, and neovascularization all contribute to the formation and stability of plaque. Let-7g, one miRNA of let-7 family, is related to retardation of the progress of vulnerable atherosclerosis plaque. First of all, let-7g induced preservation on vascular diseases through regulating on the intracellular Ca 2+ -activated protein kinase C-oxLDL-LOX-1 pathway, which resulted in reduced leukocyte adhesion to and migration across endothelium. Over expression of let-7g negatively regulated apoptosis in the ECs by targeting lectin-like oxidized LDL receptor-1(LOX-1)/CASP3 expression, therefore made the fibrous cap of plaque integrated and thick, increased the density of vascular atherosclerotic plaque. In addition, let-7g might stabilize the atherosclerotic plaque through other aspects. In this review, we focus on current and potential importance of let-7g on the stabilization of atherosclerosis plaque which might lead to the future development of an alternative strategy of CAD.

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Section: Big Nucleusmentioning

confidence: 99%

MicroRNA Let-7g and Atherosclerosis Plaque Stabilization

Yin¹,

Zhang²,

Hou³

et al. 2017

WJCD

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“…Additionally, it was shown that oxLDL-induced epigenetic suppression of FOXP3 down-regulated T regulatory cells, subsequently increasing the risk of acute coronary syndrome [260]. OxLDL raised significantly MMP-2/MMP-9-mediated migration of human aortic SMCs by epigenetic effects mediated by miRNA [261].…”

Section: Histone Deacetylasesmentioning

confidence: 99%

Enzymatic Targets in Atherosclerosis

Fuior¹,

Trusca²,

Roman³

et al. 2015

J Mol Genet Med

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Atherosclerosis, a prime cause of mortality across the developed societies, was targeted by diverse therapeutic strategies. These evolved in response to the complex etiology and evolution of the disease. Many enzymes are associated with atherosclerosis, either in the main stream of lipid biosynthesis and transport or in the collateral and intertwined pathways of oxidative stress, inflammation, vascular remodeling or chromatin stability and are therefore revised herein. Enzyme exploration led to important developments. At the beginning, there were the statins, derived as inhibitors of hydroxy-methyl-glutaryl CoA (HMG-CoA) reductase, currently used widely to decrease lipid levels. At the other end, the inhibitors of the recently discovered proprotein convertase subtilisin/kexin type 9 (PCSK9) are awaiting the validation in clinical trials with great hopes for the future. In between, one can find some palliatives, as aspirin, an inhibitor of cyclooxygenase (COX), but also many invalidated candidates. Classical pharmacological data and newer approaches, like genetic knockouts in murine atherosclerosis models, are reviewed in order to appreciate the involvement of a particular enzyme in atherogenesis. However, the pursuit of an efficacious drug has been long and, in many cases, disappointing. Conclusions can be drawn from the overview of both successes and failures, in a quest for the best.

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“…The miR-29b can also revert the aberrant methylation by targeting the DNA (cytosine-5)-methyltransferase 3a (DNMT3a) and DNMT3b genes (Fabbri et al, 2007). miR-29b plays an important role in oxLDL-mediated methylation of matrix metalloproteinase-2 (MMP-2)/ MMP-9 genes (Chen et al, 2011). (3)At the transcriptional level, the miR-29b cluster is involved in the group of interferon (IFN)-and signal transducers and activators of transcription (STAT)-regulated genes (Schmitt et al, 2012).…”

Section: The Regulation Of Mir-29bmentioning

confidence: 99%