Plasma microRNA signatures for perioperative myocardial injury.
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA604833 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR11018418.fastq.gz | Fastqsanger.gz | |||
| SRR11018419.fastq.gz | Fastqsanger.gz | |||
| SRR11018420.fastq.gz | Fastqsanger.gz | |||
| SRR11018421.fastq.gz | Fastqsanger.gz | |||
| SRR11018422.fastq.gz | Fastqsanger.gz |
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Project description:The pathophysiological mechanism(s) underlying PMI remain controversial. Small non-coding molecules that modulate gene expression may enhance the detection of myocardial injury and provide further mechanistic insight. We profiled plasma exosomal microRNA in patients who sustained PMI after elective non-cardiac surgery
2020-07-26 | GSE144777 | GEO
Project description:Background On-pump cardiac surgery provokes a predictable perioperative myocardial ischaemia–reperfusion injury which is associated with poor clinical outcomes. We determined the occurrence of time-of-the-day variation in perioperative myocardial injury in patients undergoing aortic valve replacement and its molecular mechanisms. Methods We studied the incidence of major adverse cardiac events in a prospective observational single-centre cohort study of patients with severe aortic stenosis and preserved left ventricular ejection fraction (>50%) who were referred to our cardiovascular surgery department at Lille University Hospital (Lille, France) for aortic valve replacement and underwent surgery in the morning or afternoon. Patients were matched into pairs by propensity score. We also did a randomised study, in which we evaluated perioperative myocardial injury and myocardial samples of patients randomly assigned (1:1) via permuted block randomisation (block size of eight) to undergo isolated aortic valve replacement surgery either in the morning or afternoon. We also evaluated human and rodent myocardium in ex-vivo hypoxia–reoxygenation models and did a transcriptomic analysis in myocardial samples from the randomised patients to identify the signalling pathway(s) involved. The primary objective of the study was to assess whether myocardial tolerance of ischaemia–reperfusion differed depending on the timing of aortic valve replacement surgery (morning vs afternoon), as measured by the occurrence of major adverse cardiovascular events (cardiovascular death, myocardial infarction, and admission to hospital for acute heart failure). The randomised study is registered with ClinicalTrials.gov, number NCT02812901. Findings In the cohort study (n=596 patients in matched pairs who underwent either morning surgery [n=298] or afternoon surgery [n=298]), during the 500 days following aortic valve replacement, the incidence of major adverse cardiac events was lower in the afternoon surgery group than in the morning group: hazard ratio 0·50 (95% CI 0·32–0·77; p=0·0021). In the randomised study, 88 patients were randomly assigned to undergo surgery in the morning (n=44) or afternoon (n=44); perioperative myocardial injury assessed with the geometric mean of perioperative cardiac troponin T release was significantly lower in the afternoon group than in the morning group (estimated ratio of geometric means for afternoon to morning of 0·79 [95% CI 0·68–0·93; p=0·0045]). Ex-vivo analysis of human myocardium revealed an intrinsic morning–afternoon variation in hypoxia–reoxygenation tolerance, concomitant with transcriptional alterations in circadian gene expression with the nuclear receptor Rev-Erbα being highest in the morning. In a mouse Langendorff model of hypoxia–reoxygenation myocardial injury, Rev-Erbα gene deletion or antagonist treatment reduced injury at the time of sleep-to-wake transition, through an increase in the expression of the ischaemia–reperfusion injury modulator CDKN1a/p21. Interpretation Perioperative myocardial injury is transcriptionally orchestrated by the circadian clock in patients undergoing aortic valve replacement, and Rev-Erbα antagonism seems to be a pharmacological strategy for cardioprotection. Afternoon surgery might provide perioperative myocardial protection and lead to improved patient outcomes compared with morning surgery.
2018-03-03 | GSE111351 | GEO
Project description:Current methods of stratifying patient risk of myocardial injury and stable angina rely on complex combinations of risk factors that exhibit only limited prognostic power, hence there remains a need to identify biomarkers that can be sampled non-invasively and more accurately predict patient outcomes in the clinic. In the current study, we performed comparative quantitative proteomics on whole plasma sampled from patients with stable angina (NMI), acute myocardial infarction (MI), and healthy control subjects without angina (Ctrl). We detected a total of 371 proteins with high confidence (FDR < 1%, p < 0.05), including 53 candidate biomarkers that displayed ≥ 2-fold modulated expression in patients with cardiovascular diseases (27 associated with atherosclerotic stable angina, 26 with myocardial injury). In the verification phase, we used label-free LC-MRM-MS-based targeted proteomic method to quantify and to verify the candidate biomarkers in pooled plasma, excluded peptides that were poorly distinguished from background, and then performed further validation of the remaining candidates in 49 individual plasma samples. Using this approach, we identified a final panel of 8 proteins that were both reliably and significantly modulated in disease (p < 0.05), including novel biomarkers of atherosclerotic stable angina that have been implicated in endothelial dysfunction (F10 and MST1), and previously unknown biomarkers of myocardial injury reportedly involved in either plaque destabilization (SERPINA3, CPN2, LUM) or tissue protection/repair mechanisms (ORM2, ACTG1, NAGLU). Taken together, our data showed that prognostic markers can be successfully detected in non-depleted human plasma using an iTRAQ/MRM-based discovery-validation approach, and also demonstrate that a novel panel 8 biomarkers can discriminate between the complex pathophysiologies of atherosclerotic stable angina and myocardial injury.
2018-11-06 | PXD006333 | Pride
Project description:CircRNAs have complex biological functions and are involved in the development of several cardiovascular diseases. The relationship between circRNAs and myocardial ischaemia-reperfusion injury (MIRI) is not yet clear. The aim of this study was to investigate the expression of circRNAs in rat plasma, to examine the differential expression profile of circRNAs in the plasma of MIRI rats, and to explore whether these circRNAs are potentially significant and have potential as novel markers for the diagnosis of MIRI and as therapeutic targets.
2022-12-15 | GSE220750 | GEO
Project description:Mitochondrial Creatine Kinase 2 (Ckmt2) as a Plasma-Based Biomarker for Evaluating Reperfusion Injury in Acute Myocardial Infarction
2024-10-17 | PXD055738 | Pride
Project description:Analysis of plasma circRNA expression profiles in rats with myocardial ischemia-reperfusion injury
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Project description:Many microRNA expression levels in plasma are greatly changed after mouse myocardial infarction. We aim to find out the steadily-expressed microRNAs in plasma under hypoxia and normoxia, so as to be further utilized for normalization of microRNA expression detection.
2019-01-30 | GSE124545 | GEO
Project description:We made LPS induced myocardial injury model mice, and determined the effect of recombinant human thrombomodulin against myocardial injury.
2022-09-01 | GSE131437 | GEO
Project description:BackgroundElevated plasma or serum troponin, indicating perioperative myocardial injury (PMI), is common after noncardiac surgery. However, underlying mechanisms remain unclear. Acute coronary syndrome (ACS) is associated with the early appearance of circulating microRNAs, which regulate post-translational gene expression. We hypothesised that if PMI and ACS share pathophysiological mechanisms, common microRNA signatures should be evident.MethodsWe performed a nested case control study of samples obtained before and after noncardiac surgery from patients enrolled in two prospective observational studies of PMI (postoperative troponin I/T>99th centile). In cohort one, serum microRNAs were compared between patients with or without PMI, matched for age, gender, and comorbidity. Real-time polymerase chain reaction quantified (qRT-PCR) relative microRNA expression (cycle quantification [Cq] threshold <37) before and after surgery for microRNA signatures associated with ACS, blinded to PMI. In cohort two, we analysed (EdgeR) microRNA from plasma extracellular vesicles using next-generation sequencing (Illumina HiSeq 500). microRNA-messenger RNA-function pathway analysis was performed (DIANA miRPath v3.0/TopGO).ResultsMicroRNAs were detectable in all 59 patients (median age 67 yr [61-75]; 42% male), who had similar clinical characteristics independent of developing PMI. In cohort one, serum microRNA expression increased after surgery (mean fold-change) hsa-miR-1-3p: 3.99 (95% confidence interval [CI: 1.95-8.19]; hsa-miR-133-3p: 5.67 [95% CI: 2.94-10.91]; P<0.001). These changes were not associated with PMI. Bioinformatic analysis of differentially expressed microRNAs from cohorts one (n=48) and two (n=11) identified pathways associated with adrenergic stress and calcium dysregulation, rather than ischaemia.ConclusionsCirculating microRNAs associated with cardiac ischaemia were universally elevated in patients after surgery, independent of development of myocardial injury.
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Project description:Cardiac injury following myocardial infarction exhibits a circadian pattern, yet the underlying mechanism remains unclear. To elucidate genes governing circadian variation of myocardial injury, we conducted transcriptomic profiling of left-ventricular tissues from mice or humans experiencing myocardial injury at different daytimes. Through comprehensive analyses, including transgenic mouse models and functional studies, we identified BMAL1 as a pivotal transcription factor modulating diurnal variation of myocardial injury. Remarkably, we discovered that BMAL1 regulates circadian-dependent cardiac injury by forming a transcriptionally active heterodimer with HIF2A. Substantiating this finding, we determined the cryo-EM structure of the BMAL1/HIF2F/DNA complex, revealing a previously unknown capacity for structural rearrangement within BMAL1. Furthermore, we confirmed amphiregulin (AREG) as a transcriptional target of the BMAL1/HIF2A heterodimer, critical for modulating circadian variation of myocardial injury. Finally, targeting the BMAL1/HIF2A-AREG pathway via timed AREG administration or enhancing circadian rhythm pharmacologically offered significant cardioprotection, implicating this pathway in treating ischemic heart disease.
2024-03-20 | GSE255307 | GEO