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Thymic stromal lymphopoietin modulates T cell response to improve cardiac repair post-myocardial infarction

ABSTRACT: Thymic stromal lymphopoietin modulates T cell response to improve cardiac repair post-myocardial infarction

PROVIDER: PRJNA1104986 | ENA |

REPOSITORIES: ENA

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Thymic stromal lymphopoietin modulates T cell response to improve cardiac repair post-myocardial infarction

Project description:The inflammatory response is associated with cardiac repair and ventricular remodeling after myocardial infarction (MI). The key inflammation regulatory factor thymic stromal lymphopoietin (TSLP) plays a critical role in various diseases. However, its role in cardiac repair after MI remains uncertain. In this study, we elucidated the biological function and mechanism of action of TSLP in cardiac repair and ventricular remodeling following MI. Wild-type and TSLP receptor (TSLPR)-knockout (Crlf2-/-) mice underwent MI induction via ligation of the left descending artery. TSLP expression was upregulated in the infarcted heart, with a peak observed on day 7 post-MI. TSLP expression was enriched in the cardiomyocytes of infarcted hearts, with the highest expression observed in dendritic cells. Crlf2-/- mice exhibited significantly reduced survival and worsened cardiac function, increased interstitial fibrosis and cardiomyocyte cross-sectional area, and reduced CD31+ staining, with no change in the proportion of apoptotic cardiomyocytes within the border zone. Mechanistically, a reduction in regulatory T cells and more innate immune cells and their subsets were observed in the infarcted hearts of Crlf2-/- mice, accompanied by a systemic reduction in T cell activation and proliferation. Simultaneously, RNA sequencing analysis of the infarcted hearts revealed significant downregulation of genes in Crlf2-/- mice. Our findings indicate that TSLP plays a pivotal role in regulating T cell responses, specifically T regulatory cells, thus promoting cardiac repair, which may provide a potential novel therapeutic approach for managing heart failure after MI.

2024-09-21 | GSE265931 | GEO

Bone marrow naïve B lymphocytes improve heart function after myocardial infarction

Project description:Bone marrow naïve B lymphocytes improve heart function after myocardial infarction

| PRJNA796198 | ENA

myocardial infarction in Reg3beta knock-out mice

Project description:Affymetrix microarray analysis of molecular changes after myocardial infarction. Samples of heart tissue were analyzed after myocardial infarction from WT and reg3beta knock-out mice. Samples from scar tissue and samples adjacent to the scar were analyzed. In the experiment we primarily compared infarction zone of wild-type to infarction zone of knock-out animals, and remote zone of wild-type to remote zone of knock-outs.

2015-06-29 | E-MTAB-2561 | biostudies-arrayexpress

Trem2 Macrophage Promote Cardiac Repair in Myocardial Infarction via Efferocytosis and Carbohydrate Metabolism

Project description:We want to find that the TREM2 mechanism on the Macrophages in the myocardial infarction

2022-11-15 | GSE218002 | GEO

miRNA expression data from human myocardial infarction hearts

Project description:Sexual dimorphisms are well recognized in various cardiac diseases, including myocardial infarction (MI). MI develops later in women, but once established, it contributes more persistent symptoms and higher mortality than in men. Although mRNA-level sexual dimorphism of MI have been reported, whether miRNA transcriptome also confers such dimorphism remains unknown. Comprehensive understanding of the mRNA- and miRNA-level genetic programs underlying the heart sexual dimorphisms will expectedly improve clinical outcome by facilitating the development of gender specific treatment strategies. Here, by conducting miRNA microarray analysis of human MI samples, we set out to characterize the heart sexual dimorphisms at the level of miRNA transcriptome Human tissue samples, acquired during post-mortem examination and frozen in liquid nitrogen, were provided by the department of pathology, Tokyo Metropolitan Geriatric Hospital after the approval from the ethical committee. Age- and sex-matched cohorts were selected to compare healthy hearts to those with post-MI LV remodeling. Border zone for myocardial infarction was sampled. Total RNA was extracted using Sepasol solution (Sepasol-RNA I super G, nakalai tesque, Japan), and microarray analysis was performed using Affymetrix GeneChipÂ® miRNA 3.0 Arrays

2016-01-07 | E-GEOD-76591 | biostudies-arrayexpress

Bone marrow naïve B lymphocytes improve heart function after myocardial infarction [scRNA-Seq]

Project description:Bone marrow naïve B lymphocytes improve heart function after myocardial infarction [scRNA-Seq]

| PRJNA795783 | ENA

Bone marrow naïve B lymphocytes improve heart function after myocardial infarction [RNA-Seq]

Project description:Bone marrow naïve B lymphocytes improve heart function after myocardial infarction [RNA-Seq]

| PRJNA796199 | ENA

Peripheral blood whole transcriptome in patients with acute myocardial infarction and at follow-up

Project description:There is an unmet need to develop new strategies to improve risk stratification in patients with myocardial infarction and to identify new targets for intervention. The aim of this study was to establish the unbiased peripheral blood whole transcriptome response in myocardial infarction, and to correlate it with clinical characteristics and outcome. RNA expression was determined in the acute phase of MI and at follow-up, and related to clinical phenotype and outcome.

2019-11-24 | GSE123342 | GEO

Altered gene expression pattern in peripheral blood mononuclear cells in patients with acute myocardial infarction

Project description:Despite a substantial progress in diagnosis and therapy, acute myocardial infarction (MI) is a major cause of mortality in the general population. A novel insight into the pathophysiology of myocardial infarction obtained by studying gene expression should help to discover novel biomarkers of MI and to suggest novel strategies of therapy. The aim of our study was to establish gene expression patterns in leukocytes from acute myocardial infarction patients. ST-segment elevation myocardial infarction alters expression of several groups of genes. On admission, several genes and pathways that could be directly or indirectly linked with lipid/glucose metabolism, platelet function and atherosclerotic plaque stability were affected (signaling of PPAR, IL-10, IL-6). Analysis at discharge highlighted specific immune response (upregulation of immunoglobulins). Highly significant and substantial upregulation of SOCS3 and FAM20 genes expression in the first 4-6 days of myocardial infarction in all patients is the most robust observation of our work Twenty-eight patients with ST-segment elevation myocardial infarction (STEMI) were included. The blood was collected on the 1st day of myocardial infarction, after 4-6 days, and after 6 months. Control group comprised 14 patients with stable coronary artery disease (CAD), without history of myocardial infarction. Gene expression analysis was performed with Affymetrix GeneChipM-BM-. Human Gene 1.0 ST microarrays and GCS3000 TG system.

2014-10-23 | E-GEOD-62646 | biostudies-arrayexpress

LncRNAs and mRNAs changes in border zone of myocardial infarction in rats

Project description:Comparison of both LncRNAs and mRNAs expression in the border zone of the myocardial infarction rats and the sham operation rats Border zone (BZ) of the myocardial infarction is critical to patients. Current treatments of myocardial infarction are primarily aimed to save the dying myocardial cell in the border zone. During myocardial infarction, certain changes in BZ, e.g, apoptosis, fibrosis, inflammation, etc, played an important role in deciding the survival. Impairment and recovery of BZ has been linked to gene expression changes. The aim of our study was to obtain a global expression profile of lncRNAs and mRNAs of the border zone in Wistar rats myocardial infarction, and identify the changes during myocardial infarction.

2016-12-02 | GSE90745 | GEO

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