scholarly journals MiR-21 and miR-133 levels in peripheral blood mononuclear cells associate with left ventricular diastolic dysfunction in patients with diastolic heart failure

2013 ◽  
Vol 34 (suppl 1) ◽  
pp. 68-68 ◽  
Author(s):  
M. Marketou ◽  
J. Kontaraki ◽  
E. Zacharis ◽  
F. Parthenakis ◽  
S. Margkoudakis ◽  
...  
Keyword(s):  
Heart Failure ◽  
Peripheral Blood Mononuclear Cells ◽  
Peripheral Blood ◽  
Mononuclear Cells ◽  
Diastolic Heart Failure ◽  
Left Ventricular Diastolic Dysfunction ◽  
Left Ventricular ◽  
Peripheral Blood Mononuclear ◽  
Blood Mononuclear Cells ◽  
Ventricular Diastolic Dysfunction

scholarly journals MicroRNA signatures in peripheral blood mononuclear cells of chronic heart failure patients

2010 ◽  
Vol 42 (3) ◽  
pp. 420-426 ◽  
Author(s):  
Christine Voellenkle ◽  
Jeroen van Rooij ◽  
Claudia Cappuzzello ◽  
Simona Greco ◽  
Diego Arcelli ◽  
...  
Keyword(s):  
Gene Expression ◽  
Heart Failure ◽  
Chronic Heart Failure ◽  
Peripheral Blood Mononuclear Cells ◽  
Mirna Expression ◽  
Peripheral Blood ◽  
Mononuclear Cells ◽  
Peripheral Blood Mononuclear ◽  
Control Subjects ◽  
Blood Mononuclear Cells

MicroRNAs (miRNAs) are noncoding RNAs that act as negative regulators of gene expression. Interestingly, specific alterations of miRNA expression have been found in failing hearts of different etiologies. The aim of this study was to identify the miRNA expression pattern of peripheral blood mononuclear cells (PBMCs) derived from chronic heart failure (CHF) patients affected by ischemic (ICM) and nonischemic dilated (NIDCM) cardiomyopathy. The expression profile of 257 miRNAs was assessed in 7 NIDCM patients, 8 ICM patients, and 9 control subjects by quantitative real-time PCR. Significantly modulated miRNAs were validated by using an independent set of 34 CHF patients (NIDCM = 19, ICM = 15) and 19 control subjects. Three miRNAs (miR-107, -139, and -142-5p) were downmodulated in both NIDCM and ICM patients versus control subjects. Other miRNAs were deregulated in only one of the CHF classes analyzed compared with control subjects: miR-142-3p and -29b were increased in NIDCM patients, while miR-125b and -497 were decreased in ICM patients. Bioinformatic analysis of miRNA predicted targets and of gene expression modifications associated with CHF in PBMCs indicated a significant impact of the miRNA signature on the transcriptome. Furthermore, miRNAs of both the NIDCM and the ICM signature shared predicted targets among CHF-modulated genes, suggesting potential additive or synergistic effects. The present study identified miRNAs specifically modulated in the PBMCs of NIDCM and ICM patients. Intriguingly, most of these miRNAs were previously reported as deregulated in human and/or mouse failing hearts. The identified miRNAs might have a potential diagnostic and/or prognostic use in CHF.

scholarly journals 183 Small nucleolar RNA SNORD3A: a potential new biomarker and molecular player in heart failure

2021 ◽  
Vol 23 (Supplement_G) ◽  
Author(s):  
Roberta Paolillo ◽  
Giacomo Gabriele Schiattarella ◽  
Stefania D'Apice ◽  
Christopher Holley ◽  
Alessandro Della Corte ◽  
...  
Keyword(s):  
Heart Failure ◽  
Cell Survival ◽  
Peripheral Blood Mononuclear Cells ◽  
Peripheral Blood ◽  
Mononuclear Cells ◽  
Sequencing Analysis ◽  
Peripheral Blood Mononuclear ◽  
Expression Levels ◽  
Blood Mononuclear Cells

Abstract Aims Despite optimal therapy, heart failure (HF) remains a relentless and deadly disease. Given the relative inaccessibility of myocardial human tissues, identification of circulating biomarkers mirroring myocardial pathological signalling pathways, especially in peripheral blood mononuclear cells (PBMC) is expected to be extremely relevant. Small Nucleolar RNAs (snoRNAs) have been shown to play important roles in various cellular physiological processes. However, the connection between snoRNAs and pathological dysfunction in the heart or peripheral blood mononuclear cells (PBMC) is still poorly understood. To identify novel circulating PBMC biomarkers linked to myocardial dysfunction and HF. Methods Myocardial left ventricle (LV) samples and PBMC were obtained from patients affected by ischaemic HF (HF, n = 13) undergoing heart transplantation and control donors (CD, n = 7) and analysed by RNA sequencing analysis (RNASeq). SNORD3A expression levels in the different groups were evaluated by quantitative real-time PCR. HF was induced in 8-week-old wild type C57BL/6 mice by transverse aortic constriction (TAC). Sham-operated mice (sham) were used as controls. After 12-week-TAC (12w) or sham operation, mice were anesthetized, cardiac function was analysed by echocardiography, and cardiac/PBMC samples were collected after sacrifice. In order to test the role of SNORD3A in cardiomyocyte hypoxia, H9C2 cardiomyoblasts were transfected with SNORD3A-targeted antisense oligonucleotides (ASO) and cell survival was analysed. Results RNASeq analysis identified a small set of genes differentially expressed in the heart and PBMC from HF patients. Among these, SNORD3A was up-regulated in cardiac and PBMC samples from HF patients compared to CD (Figure 1A). Similarly, in murine HF induced by 12w TAC, SNORD3A levels were increased by rtPCR, both in the heart and PBMC (Figure 1B). SNORD3A expression levels were also significantly increased in H9C2 cells exposed to in vitro hypoxia (Figure 1C). Interestingly, H9C2 transfection with SNORD3A-specific ASO significantly reduced hypoxia-induced SNORD3A up-regulation and reduced hypoxia-induced cell death (Figure 1D). Conclusions In this study, we identify SNORD3A as a novel possible biomarker in human HF, similarly up-regulated in the heart and PBMC, induced by hypoxia in vitro and modulating cell survival.

MicroRNA-208b gene expression levels as a biomarkers of left ventricular dysfunction in patients with acute myocarditis

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
M Marketou ◽  
J Kontaraki ◽  
K Fragiadakis ◽  
J Konstantinou ◽  
S Maragkoudakis ◽  
...  
Keyword(s):  
Gene Expression ◽  
Peripheral Blood Mononuclear Cells ◽  
Peripheral Blood ◽  
Mononuclear Cells ◽  
Acute Myocarditis ◽  
Left Ventricular ◽  
Peripheral Blood Mononuclear ◽  
Expression Levels ◽  
Blood Mononuclear Cells ◽  
Gene Expression Levels

Abstract Purpose MicroRNAs (miRs) play a major role in protein regulation by post-transcriptional gene expression and cell to cell interaction. Recently, they have been emerged as important modulators in cardiovascular development and disease. Our aim was to determine whether cardiac related miRs such as miR-208b was differentially expressed in peripheral blood mononuclear cells from patients with acute myocarditis. We also evaluated their expression levels in peripheral blood mononuclear cells in relation with left ventricular global longitudinal peak strain (GLPS) in those patients. Methods We assessed the expression levels of miR-208b in 55 patients with acute myocarditis (48 men, mean age 33±10 years) and 22 healthy individuals (18 men, mean age 33±9 years). Blood samples were taken on admission and miR expression levels in peripheral blood mononuclear cells were quantified by real-time reverse transcription polymerase chain reaction. All patients were also underwent an assessment with standard conventional transthoracic and a two-dimensional speckle tracking echocardiography. Results GLPS was significantly reduced in the group of myocarditis compared to healthy individuals (from −13.9±10.9% versus −22.2±6.7%, p<0.05). Myocarditis patients showed significantly higher miR-208b (28.8±16.6 versus 6.40±1.1, p<0.001) expression levels compared to control group. miR-208b gene expression levels at baseline revealed a significant negative correlation with GLPS on admission (r=−0.51, p<0.05). This correlation was independent of the patients' clinical parameters. Conclusions Our data reveal that miR-208b gene expression levels are upregulated in peripheral blood mononuclear cells from patients with acute myocarditis relative to healthy individuals. In addition, miR-208b levels have a prognostic value in the deterioration of left ventricular GLPS in those patients. Thus, miR-208b may represent a promising biomarkers in myocarditis or a potential therapeutic target in the future. Funding Acknowledgement Type of funding source: None

Abstract 4: Molecular Profile Of Peripheral Blood Mononuclear Cells In Hypertensive Adolescents With Target Organ Damage

Hypertension ◽  
2020 ◽  
Vol 76 (Suppl_1) ◽  
Author(s):  
Fnu MOHAMMED ARIF ◽  
Elaine M Urbina ◽  
Sakthivel Sadayappan ◽  
Richard Becker
Keyword(s):  
Growth Factor ◽  
Peripheral Blood Mononuclear Cells ◽  
Peripheral Blood ◽  
Mononuclear Cells ◽  
Target Organ Damage ◽  
Organ Damage ◽  
Left Ventricular ◽  
Target Organ ◽  
Peripheral Blood Mononuclear ◽  
Blood Mononuclear Cells

Introduction: Primary hypertension (PH) is a multifactorial disease influenced by genetic, epigenetic, and environmental factors. Despite the occurrence of PH-associated cardiovascular events in youth, the molecular mechanism(s) of target organ damage (TOD) are unknown. Objectives: (1) To identify an epigenetic signature and gene expression profiles in adolescents with low blood pressure (BP) and normal left ventricular mass (LVM) compared to those with high BP and high LVM; and (2) to determine novel gene targets and associated signaling pathways for future investigation and intervention. Methods and Results: A total of 397 participants (mean age 15.6 ±1.7 years, 59% male, 63% Caucasian) were enrolled across the distribution of BP. The average daytime ambulatory systolic BP recorded in healthy and hypertensive participants was 112 ±9.71 and 133 ±7.2 mmHg ( p<0.05 ) respectively. Clinical measures revealed higher body mass index (26.8 ±7.02 vs 29.6 ±7.88 Kg/m 2 ; p<0.05 ), and abnormal circulatory HDL (47.4 ±12.1 vs 43.4 ±11.7 mg/dL; p<0.05 ), glucose (87.8 ±7.98 vs 90.8 ±8.17 mg/dL; p<0.05 ), insulin (17.8 ±14.3 vs 23.7 ±19 μIU/dL; p<0.05 ), creatinine (0.718 ±0.13 vs 0.727 ±0.17 mg/dL; p<0.05 ), uric acid (5.4 ±1.63 vs 6.04 ±1.52 mg/dL; p<0.05 ), CRP (1.35 ±1.8 vs 1.92 ±2.14 mg/dL; p<0.05 ), and left ventricular hypertrophy (LVM/ht 2.7 ; 31.4 ±6.74 vs 33.5 ±7.15 g/m 2.7 ; p<0.05 ), and arterial stiffness (Pulse wave velocity; 4.83 ±0.69 vs 5.35 ±0.92 m/sec; p<0.05 ). Using peripheral blood mononuclear cells, mRNA-Seq, miRNA-Seq, and whole-genome DNA methylation analysis revealed master genes, and regulatory pathways related to BP regulation, tissue fibrosis and cardiovascular remodeling. Our study reveals a novel PH-associated TOD mechanism, showing angiogenesis inhibition mediated by VASH1 (Vasohibin-1) upregulation and downtrends in VASH2 (Vasohibin-2), VEGFC (Vascular endothelial growth factor C), HIF1α (Hypoxia-inducible factor 1-alpha), and IGF1 (Insulin Like Growth Factor 1). Moreover, VASH1 targeting miRNA hsa-miR-30e-5p is inversely regulated. Conclusion: Angiogenesis inhibition in the presence of common demographic and clinical intermediate-phenotypes may contribute to the development of TOD in hypertensive youth.

P5561MicroRNA-208b gene expression levels as a biomarkers of left ventricular dysfunction in patients with acute myocarditis

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
M Marketou ◽  
J Kontaraki ◽  
K Fragiadakis ◽  
J Konstantinou ◽  
S Maragkoudakis ◽  
...  
Keyword(s):  
Gene Expression ◽  
Peripheral Blood Mononuclear Cells ◽  
Peripheral Blood ◽  
Mononuclear Cells ◽  
Acute Myocarditis ◽  
Left Ventricular ◽  
Peripheral Blood Mononuclear ◽  
Expression Levels ◽  
Blood Mononuclear Cells ◽  
Gene Expression Levels

Abstract Purpose MicroRNAs (miRs) play a major role in protein regulation by post-transcriptional gene expression and cell to cell interaction. Recently, they have been emerged as important modulators in cardiovascular development and disease. Our aim was to determine whether cardiac related miRs such as miR-208b was differentially expressed in peripheral blood mononuclear cells from patients with acute myocarditis. We also evaluated their expression levels in peripheral blood mononuclear cells in relation with left ventricular global longitudinal peak strain (GLPS) in those patients. Methods We assessed the expression levels of miR-208b in 45 patients with acute myocarditis (38 men, mean age 31±10 years) and 22 healthy individuals (18 men, mean age 33±9 years). Blood samples were taken on admission and miR expression levels in peripheral blood mononuclear cells were quantified by real-time reverse transcription polymerase chain reaction. All patients were also underwent an assessment with standard conventional transthoracic and a two-dimensional speckle tracking echocardiography. Results GLPS was significantly reduced in the group of myocarditis compared to healthy individuals (from −13.7 ± −7.9% versus −22.2±6.7%, p<0.05). Myocarditis patients showed significantly higher miR-208b (28.5±6.6 versus 6.40±1.1, p<0.001) expression levels compared to control group. miR-208b gene expression levels at baseline revealed a significant negative correlation with GLPS on admission (r=−0.51, p<0.05). This correlation was independent of the patients' clinical parameters. Conclusions Our data reveal that miR-208b gene expression levels are upregulated in peripheral blood mononuclear cells from patients with acute myocarditis relative to healthy individuals. In addition, miR-208b levels have a prognostic value in the deterioration of left ventricular GLPS in those patients. Thus, miR-208b may represent a promising biomarkers in myocarditis or a potential therapeutic target in the future.

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