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Gene expression profiling reveals potential prognostic biomarkers associated with the progression of heart failure

ABSTRACT: Heart failure (HF) is the most common cause of morbidity and mortality in the developed countries, especially considering the present demographic tendencies in those populations. We identified biologically relevant transcripts that are significantly altered in the early phase of myocardial infarction (MI) and are associated with the development of post-myocardial infarction HF.

ORGANISM(S): Homo sapiens

PROVIDER: GSE59867 | GEO | 2015/05/21

SECONDARY ACCESSION(S): PRJNA256954

REPOSITORIES: GEO

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Gene expression profiling reveals potential prognostic biomarkers associated with the progression of heart failure

Project description:Heart failure (HF) is the most common cause of morbidity and mortality in the developed countries, especially considering the present demographic tendencies in those populations. We identified biologically relevant transcripts that are significantly altered in the early phase of myocardial infarction (MI) and are associated with the development of post-myocardial infarction HF. We collected peripheral blood samples from patients (n=111) with ST-segment elevation myocardial infarction (STEMI) at four time points (admission, discharge, 1 month after MI, and 6 months after MI). Control group comprised patients (n=46) with a stable coronary artery disease and without a history of myocardial infarction. Affymetrix HuGene 1.0 ST arrays were used to analyze mRNA levels in periperal blood mononuclear cells (PBMCs) isolated from the study and control groups. Samples from the first three time points were compared with the samples from the same patients collected 6 months after MI (stable phase) and with the control group. Additionaly, based on plasma NT-proBNP level and left ventricular ejection fraction parameters the STEMI patients were divided into HF and non-HF groups.We attempted to identify transcripts whose differential expression on the 1st day of myocardial infarction predicted which patients would develop symptoms of HF during the 6 months of follow-up. For this purpose, we compared the microarray results for samples collected on admission for the HF group versus the non-HF group.

2015-05-21 | E-GEOD-59867 | biostudies-arrayexpress

Dapagliflozin protects against chronic heart failure in mice via inhibiting macrophage-mediated inflammation, independent of SGLT2 [RNA-Seq]

Project description:The specific mechanism of sodium-glucose cotransporter 2 (SGLT2) inhibitor in heart failure (HF) needs to be elucidated. In this study, we use SGLT2 global knockout (SGLT2-KO) mice to assess the mechanism of SGLT2 inhibitor on HF. Dapagliflozin ameliorates both myocardial infarction (MI)-and transverse aortic constriction (TAC) -induced HF. Global SGLT2-deficiency doesn’t exert protection against adverse remodeling in both MI- and TAC-induced HF models. Dapagliflozin blurs MI- and TAC-induced HF phenotypes in SGLT2-KO mice. Dapagliflozin causes major changes in cardiac fibrosis and inflammation. Based on single-cell RNA sequencing dapagliflozin causes significant differences in the gene expression profile of macrophages and fibroblasts. Moreover, dapagliflozin directly inhibites macrophage inflammation, thereby suppressing cardiac fibroblasts activation. The cardio-protection of dapagliflozin is blurred in mice treated with a C-C chemokine receptor type 2 (CCR2) antagonist. Taken together the protective effects of dapagliflozin against HF are independent of SGLT2, macrophage inhibition is the main target of dapagliflozin against HF.

2023-11-14 | GSE247062 | GEO

Transcriptional profiling of left ventricle and peripheral blood cells in rats with post-myocardial infarction

Project description:Myocardial infarction (MI) often results in left ventricular (LV) remodeling followed by heart failure (HF). It is of great clinical importance to understand the molecular mechanisms that trigger transition from compensated LV injury to HF and to identify relevant diagnostic biomarkers. In this study, we performed transcriptional profiling of LVs in rats with a wide range of experimentally induced infarct sizes and of peripheral blood mononuclear cells (PBMCs) in animals that developed HF. We used microarrays to investigate gene expression in the left ventricle (LV) accompanying myocardial infarction and concomitant heart failure (HF) in a well validated model of post-infarcted heart failure and to evaluate their reflection in peripheral blood mononuclear cells (PBMCs) Myocardial infarction (MI) was induced in male Wistar rats by ligation of the proximal left coronary artery. The sham-operated group (control group) was subjected to the same protocol, except that the suture was not tied around the proximal left coronary artery. Sham-operated rats (n=6) and rats with small (n=6), moderate (n=6), and large (n=5) MI size were included into the experiment two months after the operation. Then, left ventricules and blood samples were obtained for RNA extraction and hybridization on Affymetrix microarrays. Microarrays were used to compare the LV and PBMCs transcriptomes of control and experimental animals. The development of heart failure was estimated by echocardiography and catheterization.

2013-11-15 | E-GEOD-47495 | biostudies-arrayexpress

Bulk RNA-seq of mouse heart tissue for analyzing gene expression of myocardial infarction progression

Project description:Myocardial infarction (MI) is a leading cause of heart failure (HF), which is associated with morbidity and mortality worldwide. Understanding the molecular characteristics of of MI is of significance for treating post-MI HF. In this study, RNA-seq was performed on heart tissue from mouse models at multiple time points (sham, 7d and 28d) to explore genetic features that influence MI progression.

2023-07-04 | GSE236374 | GEO

Proteomics of JHS samples identifies proteins associated with heart failure

Project description:RELEVANCE: Identifying early plasma protein biomarkers that predict the development of heart failure (HF) following myocardial infarction (MI) will help to stratify at risk subjects and provide insight into more effective therapeutic strategies. OBJECTIVE/HYPOTHESIS: The goal of this study was to determine markers of HF in African Americans, using plasma samples collected before the development of symptoms. We propose that early plasma glycoprotein changes will link to later development of heart failure. ApolipoproteinF will be the strongest indicator. METHODS: Plasma samples from a subset of Jackson Heart Study participants with a history of MI but without prevalent heart failure (HF) at visit 2 (2005-2008) were analyzed by glycoproteomics. Individuals were grouped into those who experienced subsequent HF hospitalization after visit 2 (n=15; 3 men/ 12 women) and those without HF hospitalization through 2012 (n=45; 24 men/ 21 women). N-linked plasma glycopeptides were quantified by solid-phase extraction coupled to mass spectrometry and identified using RefSeq and SwissProt. Proteins were mapped for biological processes and functional pathways using Ingenuity Pathway Analysis (IPA) and linked to clinical characteristics.

2018-08-30 | PXD009870 | Pride

Transcriptomic profiling of chronic infarcted pig hearts

Project description:Myocardial infarction (MI) is the leading cause for hear failure (HF). Following MI, the non-infarcted region of left ventricle (LV) is critical for maintaining heart function, and disruption of the LV contributes greatly to post-MI HF. Transcriptomic profiling by high-throughput sequencing was performed in a chronic HF pig model, to explore the molecular changes in the post-MI LV related to cardiovascular deterioration. Samples were taken from heart tissue of MI-induced pigs and from control pigs not subjected to MI. Regions of the heart where samples were taken included the site of ischemia (LV ischemia), area bordering ischemia (LV border), area remote to ischemia (LV remote) and the right ventricle (RV).

2021-10-04 | E-MTAB-8856 | biostudies-arrayexpress

Uncovering potential lncRNAs and mRNAs in progression from acute myocardial infarction to myocardial fibrosis to heart failure

Project description:Background: In spite of modern reperfusion therapies, morbidity and mortality of heart failure (HF) post myocardial infarction (MI) remain elevated. The aim of this study was to identify potential long non-coding RNAs (lncRNAs) and mRNAs in progression from acute myocardial infarction (AMI) to myocardial fibrosis (MF) to HF. Methods: Firstly, blood samples from 3 AMI patients, 3 MF patients and 3 HF patients were used for RNA sequencing. Secondly, differentially expressed lncRNAs and mRNAs were obtained in MF vs AMI and HF vs MF, followed by functional annotation of common differentially expressed mRNAs between two groups. Thirdly, interaction networks of lncRNA-nearby targeted mRNA and lncRNA-co-expressed mRNA were constructed in MF vs AMI and HF vs MF. Finally, expression validation and diagnostic capability analysis of selected lncRNAs and mRNAs were performed. Results: Several lncRNA-co-expressed/nearby targeted mRNAs pairs including AC005392.3/AC007278.2-IL18R1, AL356356.1/AL137145.2-PFKFB3 and MKNK1-AS1/LINC01127-IL1R2 were identified. Several signaling pathways including TNF signaling pathway and cytokine-cytokine receptor interaction (involved IL18R1), fructose and mannose metabolism and HIF-1 signaling pathway (involved PFKFB3), hematopoietic cell lineage and fluid shear stress and atherosclerosis (involved IL1R2) and estrogen signaling pathway (involved FKBP5) were screened out. FKBP5, IL1R2, IRAK3, LRG1, RNASE1 and PLAC4 had a potential diagnostic value for HF.

2021-07-13 | GSE168281 | GEO

mRNA Expression Data from murine Medial Prefrontal Cortex and Hippocampus at baseline, 64 hours post-MI, and 8 weeks post-MI in Clock∆19/∆19 and WT C57Bl/6 mice

Project description:Male Clock∆19/∆19 and WT C57Bl/6 mice were randomized into 3 groups: i) baseline, ii) short-term post-myocardial infarction (MI; 64h post-MI), iii) long-term post-MI (heart failure, HF; 8 weeks post-MI). Medial prefrontal cortex (mPFC) and hippocampus brain regions were collected at ZT19 (waketime). The microarray approach allows the investigation of transcriptome-wide gene expression changes in brain regions from Clock∆19/∆19 and WT mice at baseline, post-MI, and in HF.

2019-01-05 | GSE124670 | GEO

Transcriptional profiling of left ventricle and peripheral blood cells in rats with post-myocardial infarction

2013-11-15 | GSE47495 | GEO

Comprehensive analysis of the RNA transcriptome expression profiles and construction of the ceRNA network in heart failure patients

Project description:Comprehensive analysis of the RNA transcriptome expression profiles and construction of the ceRNA network in heart failure patients with therapeutic heterogeneity of sacubitril/valsartan after acute myocardial infarction Patients after Acute Myocardial Infarction Sacubitril/valsartan has a noteworthy advantage in improving ventricular remodelling, as well as reducing cardiovascular mortality and the rate of heart failure (HF) readmission. However, clinically, some patients with HF still have low sensitivity to sacubitril/valsartan, indicating sacubitril/valsartan resistance (SVR).

2022-12-31 | GSE212181 | GEO

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