Purpose MicroRNAs (miRs) are implicated in various cardiovascular pathologies and are promising diagnostic and therapeutic targets. miR-21 plays a critical role in the regulation of inflammation and cardiac fibrosis. In this study, we evaluated miR-21 expression levels in peripheral blood mononuclear cells from patients with acute myocarditis compared to healthy individuals and explored their diagnostic potential as predictor of myocardial damage. Methods We assessed the expression levels of miR-21 in 55 patients with acute myocarditis (40 men, mean age 30±12 years) and 20 healthy individuals (15 men, mean age 30±9 years). Blood samples were taken on admission and miR-21 expression levels in peripheral blood mononuclear cells were quantified by real-time reverse transcription polymerase chain reaction. Plasma high sensitive troponine (TnI) was measured by immunoassay and a value above the laboratory reference range (11.6 pg/ml) was considered elevated. Results Myocarditis patients showed significantly higher troponine levels compared to healthy individuals (256.59±94.9 versus 11.9±9.01, p<0.001). miR-21 expression levels in peripheral blood mononuclear cells were significantly elevated in the myocarditis group compared to the control group (47.01±18.3 versus 3.8±2.2, p=0.02). In addition, miR-21 expression levels in peripheral blood mononuclear cells revealed a significant correlation with troponine levels in those patients (r=0.55, p<0.001) Conclusions Our data reveal that miR-21 is upregulated in peripheral blood mononuclear cells from patients with acute myocarditis relative to healthy individuals and is significantly correlated with myocardial damage in those patients. Our findings indicate that miR-21 may be involved in the pathophysiology of myocarditis and represent promising biomarker in the disease.
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
Background:We tested the hypothesis that combined xenogenic (from minipig) adipose-derived mesenchymal stem cell (ADMSC) and ADMSC-derived exosome therapy could reduce brain-infarct zone (BIZ) and enhance neurological recovery in rat after acute ischemic stroke (AIS) induced by 50-min left middle cerebral artery occlusion. Methods and results: Adult-male Sprague-Dawley rats (n=60) were divided equally into group 1 (sham-control), group 2 (AIS), group 3 [AIS-ADMSC (1.2×106 cells)], group 4 [AIS-exosome (100μg)], and group 5 (AIS-exosome-ADMSC). All therapies were provided intravenously at 3h after AIS procedure. BIZ determined by histopathology (by day-60) and brain MRI (by day-28) were highest in group 2, lowest in group 1, higher in groups 3 and 4 than in group 5, but they showed no difference between groups 3 and 4 (all p<0.0001). By day-28, sensorimotor functional results exhibited an opposite pattern to BIZ among the five groups (p<0.005). Protein expressions of inflammatory (inducible nitric oxide synthase/tumor necrosis factor-α/nuclear factor-κB/interleukin-1β/matrix metalloproteinase-9/plasminogen activator inhibitor-1/RANTES), oxidative-stress (NOX-1/NOX-2/oxidized protein), apoptotic (caspase-3/ Poly-ADP-ribose polymerase), and fibrotic (Smad3/transforming growth factor-β) biomarkers, and cellular expressions of brain-damaged (γ-H2AX+/ XRCC1-CD90+/p53BP1-CD90+), inflammatory (CD11+/CD68+/glial fibrillary acid protein+) and brain-edema (aquaporin-4+) markers showed a similar pattern of BIZ among the groups (all p<0.0001). Conclusion: Xenogenic ADMSC/ADMSC-derived exosome therapy was safe and offered the additional benefit of reducing BIZ and improving neurological function in rat AIS. Background: Myocarditis is one of the major causes of heart failure and sudden death in young adults. Conservative therapies are not effective for all patients. Consequently, the improvement of already existing therapies is essential. For this purpose, still unknown molecular targets triggering the disease have to be identified. One such molecular target is the immunoproteasome (IP), which is a multicatalytic protease predominantly expressed in cells of hematopoietic origin. The catalytic activity of this protease is restricted to the three β subunits low-molecular-weight protein 2 and 7 (LMP 2 and 7) and Mecl-1. By yet undetermined mechanisms, IP function contributes to disease onset in autoimmune disorders like rheumatoid arthritis and inflammatory bowel disease. Purpose: In this study, we aimed to investigate the role of LMP2 and LMP7 for disease manifestation in autoimmune myocarditis. Methods: To investigate the role of LMP2 and LMP7 in the experimental autoimmune myocarditis (EAM) animal model, LMP2−/−, LMP7−/− as well as their respective wild-type (wt) littermates were immunised with 150 μg troponin I (TnI) peptide in conjunction with complete Freunds adjuvans (CFA). Echocardiographic analyses were performed and inflammation score, hs-TnT level and TnI peptide antibody titres of sera were determined. Results: Heart ...
Background:The objective of this study was to identify prognostic indicators in patients with inflammatoric cardiomyopathy (CMi) on endomyocardial biopsy (EMB). Methods: Between 2007 and 2012 all consecutive patients with CMi on EMB were retrospectively analyzed. The combined primary endpoint was cardiac death, survived sudden cardiac death, appropriate ICD shock, heart transplantation, and LVAD implantation. Results: 503 consecutive patients (mean age 58±12 years, 73% male) were available for analysis. During mean 3.6±2.4 years of follow-up (FU), 40 patients (8.6%) reached the primary endpoint, which was in 14 patients cardiac death (cardiac mortality 3.0%). Independent predictors for the primary endpoint were age ≥50 years, symptoms of congestive heart failure, and duration of symptoms ≤28 days. A risk stratification approach based on the results of the multivariate analysis demonstrated that absence of signs and/or symptoms of congestive heart failure in younger (<50 years) patients with longer (>28 days) duration of disease appear to have an excellent prognosis with 100% survival and no events during FU (Figure 1). In contrast, presence of signs and/or symptoms of heart failure in older (≥50 years) patients with short duration (≤28 days) of the disease, results in a primary end-point occurrence of 35.9% during FU. Conclusions:For patients with biopsy-proven inflammatoric cardiomyopathy, symptoms of heart failure, short duration of disease, and older age, but not immunohistology or viral genome detection, were related to poor outcome.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.