Circulating miR-155, miR-145 and let-7c as diagnostic biomarkers of the coronary artery disease

Faccini, Julien; Ruidavets, Jean‐Bernard; Cordelier, Pierre; Martins, Frédéric; Maoret, Jean‐José; Bongard, Vanina; Ferrières, Jean; Roncalli, Jérôme; Elbaz, Meyer; Vindis, Cécile

doi:10.1038/srep42916

Cited by 119 publications

(96 citation statements)

References 36 publications

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“…However, the level of miR‐155 in PBMC or plasma was found to be lower in patients with UA and acute myocardial infarction than in patients with chest pain syndrome, whereas there were no significant differences between patients with stable CAD and chest pain syndrome . More recently, Faccini et al, based on an exploratory miRNA microarray in age‐matched CAD patients and controls and on literature mining, selected miR‐155, miR‐145, let‐7c, and miR‐92 as candidates. They further validated the expression of these four miRNAs in a larger group and showed a significant decrease in let‐7c, miR‐155, and miR‐145 expression, and similar expression of miR‐92a levels in 69 patients with CAD compared with 32 control subjects.…”

Section: Discussionmentioning

confidence: 99%

Peripheral blood mononuclear cell microRNAs in coronary artery disease

Sanlialp

Dodurga

Uludag³

et al. 2019

J of Cellular Biochemistry

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The accuracy of risk prediction for coronary artery disease can be improved with the use of novel molecular or genetic biomarkers. In this study, we investigated the difference of five selected microRNAs (miR or miRNA) in patients with coronary artery disease (CAD) and controls, assessed by coronary angiography. The study population consisted of 85 subjects, aged between 18 and 75 years and underwent invasive coronary angiography. Subjects with more than 30% stenosis in at least one coronary artery, patients with a history of prior percutaneous coronary intervention or coronary by‐pass surgery were allocated to the patient group; whereas the subjects without at least 30% stenosis consisted the control group. Groups were similar in age, presence of hypertension, and smoking status. However, the proportion of males and subjects taking angiotensin‐converting enzyme inhibitors or angiotensin receptor blockers, beta blockers, nitrates, and statins were higher in the patient group. miR‐221 and miR‐155 were downregulated (P = .02 and .001, respectively), while miR‐21 levels were significantly increased (P = .003) in the patient group compared to controls. Changes in miR‐145 and miR‐126 did not reach statistical significance (P > .05). miRNA‐ 21, miR‐155, and miR‐221 were differentially expressed between the patients and controls. miRNAs are promising biomarkers for CAD diagnosis, however, this requires further research with larger groups.

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Section: Discussionmentioning

confidence: 99%

Peripheral blood mononuclear cell microRNAs in coronary artery disease

Sanlialp

Dodurga

Uludag³

et al. 2019

J of Cellular Biochemistry

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“…Among those identified were miR-130a and miR-15B, which are known to regulate Wnt signalling [40,41] and are identified as biomarker of atherosclerosis obliterans [42]. miR-154 was found to be a biomarker for CAD [43]; and miR216A has roles in osteogenesis and cholesterol efflux via PI3K/AKT pathway [44,45]. Some of the microRNAs identified are also implicated in the pro-fibrotic TGF-β signalling pathway and found to be involved in fibrosis by targeting extracellular matrix structural proteins and enzymes involved in cellular remodeling.…”

Section: Discussionmentioning

confidence: 99%

Gene Expression and Proteomic Profiling of Lp (a)-Induced Signalling Pathways in Human Aortic Valve Interstitial Cells

Yu¹,

Kapur²,

Hamid³

et al. 2018

J Pharmacogenomics Pharmacoproteom

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Aortic valve stenosis is one of the most common valve diseases in the world for which there is currently no pharmacological treatment to prevent or halt disease progression. Recent genetic research has demonstrated a causal association between elevated blood levels of lipoprotein (a) (Lp (a)) and aortic valve calcification, however, the mechanisms by which Lp (a) contributes to aortic valve calcification and stenosis, is unknown. In the present study, we aimed at determining Lp (a)-induced changes in human aortic valve interstitial cells using an integrated bioinformatics approach. The Lp (a)-induced cellular pathways were analysed using microarray gene expression and proteomic data from non-stenotic human aortic valve interstitial cells. Lp (a) treatment induced osteogenic differentiation, extracellular remodeling, extracellular vesicles biogenesis, and apoptosis of human aortic valve interstitial cells. In particular, the Wnt/ β-catenin signalling pathway, a known calcification pathway contributing to aortic valve stenosis, was differentially expressed compared to non-treated cells. Lp (a) also induced the expression of 14-3-3 proteins known to regulate various signalling pathway relevant to aortic valve disease. Elucidating the mechanisms and molecular players that Lp (a) induces in the early stages of the disease to initiate aortic valve calcification could provide insight into potential pharmacological targets for the treatment of this debilitating disease.

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“…Let7-c is elevated in endothelial to mesenchymal transition (EndMT) (32). It shows reduced expression in coronary artery disease patients as opposed to control (44). Let7-i limits the toll like receptors like TLR4 by targeting it.…”

Section: Discussionmentioning

confidence: 99%

Modulation of ADARs mRNA expression in congenital heart defect patients

Altaf

Vesely

et al. 2018

Preprint

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27Adenosine (A) to inosine (I) RNA editing, is a hydrolytic deamination reaction catalyzed by 28 adenosine deaminase (ADAR) acting on RNA enzymes. RNA editing is a molecular process that 29 involves the post-transcriptional modification of RNA transcripts. Interestingly, few studies have 30 been carried out to determine the role of RNA editing in vascular disease. The current study 31 found that in blood samples positive for congenital heart disease (CHD) ADAR1 and ADAR2 32 expression change at RNA level was opposite to each other. That is, an increase of ADAR1 33 mRNA was noticed in human CHD cases, whereas ADAR2 mRNA was vastly down-regulated. 34The increase in ADAR1 may be explained by the stress induced by CHD. The dramatic decrease 35 in ADAR2 in CHD cases was unexpected and prompted further investigation into its effects on 36 the heart. Therefore we performed expression analysis on a microarray data encompassing 37 ischemic and non-Ischemic cardiomyopathy patient myocardial tissues. A strong down-38 regulation of ADAR2 was observed in both ischemic and especially non-ischemic cases. 39However, ADAR1 showed a mild increase in the case of non-ischemic myocardial tissues. To 40 further explore the role of ADAR2 with respect to heart physiology. We selected a protein 41 coding gene filamin B (FLNB). FLNB is known to play an important role in heart development. 42Although there were no observable changes in its expression, the editing levels of FLNB 43 dropped dramatically in ADAR2 -/mice. We also performed miRNA profiling from ADAR2 -/-44 mice heart tissue revealed a decrease in expression of miRNAs. It is established that aberrant 45 expression of these miRNAs is often associated with cardiac defects. This study proposes that 46 sufficient amounts of ADAR2 might play a vital role in preventing cardiovascular defects. 47 48 KEYWORDS 49

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Circulating miR-155, miR-145 and let-7c as diagnostic biomarkers of the coronary artery disease

Cited by 119 publications

References 36 publications

Peripheral blood mononuclear cell microRNAs in coronary artery disease

Peripheral blood mononuclear cell microRNAs in coronary artery disease

Gene Expression and Proteomic Profiling of Lp (a)-Induced Signalling Pathways in Human Aortic Valve Interstitial Cells

Modulation of ADARs mRNA expression in congenital heart defect patients

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