From heart to toe: Heart's contribution on peripheral microRNA levels

Boeckel, Jes‐Niels; Reis, Sophia; Leistner, David M.; Thome, Claudia; Zeiher, Andreas M.; Fichtlscherer, Stephan; Keller, Till

doi:10.1016/j.ijcard.2014.01.082

Cited by 9 publications

(7 citation statements)

References 9 publications

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“…21 Furthermore, a study examining a range of vascular miRNAs demonstrated that most miRNAs were well correlated, with no significant difference between coronary sinus and peripheral venous blood. 56 In our study, expression of all 51 miRNAs were comparable across sampling sites, suggesting that they are altered systemically rather than locally, according to disease state and treatment effect, suggesting that venous sampling alone is sufficient to track disease activity or treatment response. However, there were 4 of the 51 miRNAs that exhibited significantly altered transcoronary (CS-A) concentration gradients.…”

Section: Mirna Expression Across Sampling Sites and The Coronary Bedsupporting

confidence: 51%

A MicroRNA Signature in Acute Coronary Syndrome Patients and Modulation by Colchicine

Barraclough

Joglekar

Januszewski

et al. 2020

J Cardiovasc Pharmacol Ther

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Background: Circulating microRNAs (miRNAs) may play a pathogenic role in acute coronary syndromes (ACS). It is not yet known if miRNAs dysregulated in ACS are modulated by colchicine. We profiled miRNAs in plasma samples simultaneously collected from the aorta, coronary sinus, and right atrium in patients with ACS. Methods: A total of 396 of 754 miRNAs were detected by TaqMan real-time polymerase chain reaction from EDTA-plasma in a discovery cohort of 15 patients (n = 3 controls, n = 6 ACS standard therapy, n = 6 ACS standard therapy plus colchicine). Fifty-one significantly different miRNAs were then measured in a verification cohort of 92 patients (n = 13 controls, n = 40 ACS standard therapy, n = 39 ACS standard therapy plus colchicine). Samples were simultaneously obtained from the coronary sinus, aortic root, and right atrium. Results: Circulating levels of 30 of 51 measured miRNAs were higher in ACS standard therapy patients compared to controls. In patients with ACS, levels of 12 miRNAs (miR-17, -106b-3p, -191, -106a, -146a, -130a, -223, -484, -889, -425-3p, -629, -142-5p) were lower with colchicine treatment. Levels of 7 of these 12 miRNA were higher in ACS standard therapy patients compared to controls and returned to levels seen in control individuals after colchicine treatment. Three miRNAs suppressed by colchicine (miR-146a, miR-17, miR-130a) were identified as regulators of inflammatory pathways. MicroRNAs were comparable across sampling sites with select differences in the transcoronary gradient of 4 miRNA. Conclusion: The levels of specific miRNAs elevated in ACS returned to levels similar to control individuals following colchicine. These miRNAs may mediate ACS (via inflammatory pathways) or increase post-ACS risk, and could be potentially used as biomarkers of treatment efficacy.

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Section: Mirna Expression Across Sampling Sites and The Coronary Bedsupporting

confidence: 51%

A MicroRNA Signature in Acute Coronary Syndrome Patients and Modulation by Colchicine

Barraclough

Joglekar

Januszewski

et al. 2020

J Cardiovasc Pharmacol Ther

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“…The transcardiac gradient of specific miRNAs has been previously reported in the literature in healthy hearts (miRNAs studied: miR‐34a, miR‐92a‐3p, miR‐155, miR‐378‐3p, miR‐1‐3p, miR‐133a‐3p, and miR‐499), CAD (miR‐133a, miR‐499, miR‐208a, miR‐126, miR‐92a, miR‐155, and miR‐233), coronary endothelial dysfunction (miR‐17, miR‐92a, miR‐126, miR‐34, miR‐181b, miR‐221, miR‐222, miR‐208, miR‐133, miR‐21, miR‐145, and miR‐155), and heart failure (miR‐29b, miR‐133a, and miR‐423) . Similarly to our study, Goldraich and colleagues analysed samples collected from the coronary sinus of healthy and failing hearts.…”

Section: Discussionmentioning

confidence: 74%

“…Similarly to our study, Goldraich and colleagues analysed samples collected from the coronary sinus of healthy and failing hearts. Our study, however, had several strengths compared with previous transcardiac miRNA gradient studies, regardless of the health or disease state analysed . First, we used a global normalization method instead of exogenous spike‐in (cel‐miR‐39) normalization.…”

Section: Discussionmentioning

confidence: 99%

The transcardiac gradient of cardio‐microRNAs in the failing heart

Marques

Vizi

Khammy

et al. 2016

European J of Heart Fail

165

108

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Aims Differential microRNA expression in peripheral blood has been observed in patients with heart failure, suggesting their value as potential biomarkers and likely contributors to disease mechanisms. In the present study, we aimed to evaluate the transcardiac gradient of 84 cardio‐microRNAs in healthy and failing hearts to determine which microRNAs are released or absorbed by the myocardium in heart failure. Methods and results Eight healthy volunteers and nine patients with congestive heart failure were included. Arterial and coronary sinus blood samples were collected, and microRNAs were extracted. The expression of microRNAs was analysed using real‐time PCR by the miScript miRNA PCR Array Human Cardiovascular Disease. In coronary sinus samples, the microRNAs miR‐16‐5p, miR‐27a‐3p, miR‐27b‐3p, miR‐29b‐3p, miR‐29c‐3p, miR‐30e‐5p, miR‐92a‐3p, miR‐125b‐5p, miR‐140‐5p, miR‐195‐5p, miR‐424‐5p, and miR‐451a were significantly down‐regulated, and let‐7a‐5p, let‐7c‐5p, let‐7e‐5p, miR‐23b‐3p, miR‐107, miR‐155‐5p, miR‐181a‐5p, miR‐181b‐5p and miR‐320a were up‐regulated in heart failure. Left ventricular filling pressure was negatively correlated with miR‐195, miR‐16, miR‐29b‐3p, miR‐29c‐3p, miR‐451a, and miR‐92a‐3p. The failing heart released let‐7b‐5p, let‐7c‐5p, let‐7e‐5p, miR‐122‐5p, and miR‐21‐5p, and absorbed miR‐16‐5p, miR‐17‐5p, miR‐27a‐3p, miR‐30a‐5p, miR‐30d‐5p, miR‐30e‐5p, miR‐130a‐3p, miR‐140‐5p, miR‐199a‐5p, and miR‐451a. In silico analyses suggest that the transcardiac gradient of microRNAs in heart failure may target pathways related to heart disease. Conclusion We determined the transcardiac gradient of cardio‐microRNAs in failing hearts, which supports the use of these microRNAs as potential biomarkers. The microRNAs described here may have a role in the pathophysiology of heart failure as they might be involved in pathways related to disease progression, including fibrosis.

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“…However, miRNAs that are up regulated in heart tissue also manifest in the circulation during less traumatic chronic cardiovascular conditions. MiR-1 and miR-133a are elevated in the circulation with unstable angina, cardiomyopathy [61] and coronary atherosclerosis [9, 35]; miR-208a tends to be elevated with stable coronary artery disease [35]; miR-21 and miR-29 are up regulated with ventricular fibrosis [89, 112] and hypertrophic cardiomyopathy [89]; miR-499 and miR-208b are increased with viral myocarditis [18]; and miR-21 is up regulated with various degrees of diagnosed heart failure [13, 46, 101] as well as coronary artery disease [50]. Most recently, a panel of circulating miRNAs sensitive enough to distinguish between chronic heart failure with preserved versus reduced ejection fraction was identified, and circulating miR-221 and miR-328 levels increased the discriminatory power of circulating B-type natriuretic peptide for assessing heart failure [116].…”

Section: Mirnas Heart Failure and Skeletal Musclementioning

confidence: 99%

“…Other compounds such as myostatin released from cardiac tissue during heart failure can strongly regulate skeletal muscle mass [52]. Emerging evidence suggests that diseased cardiac tissue is a major source of circulating miRNAs [9] and that miRNAs (via extracellular vesicles or some other mechanism) participate in intercellular communication [3]. Further research on how miRNAs are released from cardiac tissue, under what conditions they are released, how skeletal muscle is potentially targeted by extracellular vesicles/miRNAs, and the specific effects of these miRNAs in skeletal muscle is warranted.…”

Section: Mirnas Heart Failure and Skeletal Musclementioning

confidence: 99%

MicroRNAs, heart failure, and aging: potential interactions with skeletal muscle

Murach

McCarthy

2016

Heart Fail Rev

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MicroRNAs (miRNAs) are small noncoding RNAs that regulate gene expression by targeting mRNAs for degradation or translational repression. MiRNAs can be expressed tissue specifically and are altered in response to various physiological conditions. It has recently been shown that miRNAs are released into the circulation, potentially for the purpose of communicating with distant tissues. This manuscript discusses miRNA alterations in cardiac muscle and the circulation during heart failure, a prevalent and costly public health issue. A potential mechanism for how skeletal muscle maladaptations during heart failure could be mediated by myocardium-derived miRNAs released to the circulation is presented. An overview of miRNA alterations in skeletal muscle during the ubiquitous process of aging and perspectives on miRNA interactions during heart failure are also provided.

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From heart to toe: Heart's contribution on peripheral microRNA levels

Cited by 9 publications

References 9 publications

A MicroRNA Signature in Acute Coronary Syndrome Patients and Modulation by Colchicine

A MicroRNA Signature in Acute Coronary Syndrome Patients and Modulation by Colchicine

The transcardiac gradient of cardio‐microRNAs in the failing heart

MicroRNAs, heart failure, and aging: potential interactions with skeletal muscle

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