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Inhibition of DYRK1A promotes cardiomyocyte proliferation and heart repair after myocardial infarction

ABSTRACT: Inhibition of DYRK1A promotes cardiomyocyte proliferation and heart repair after myocardial infarction

PROVIDER: PRJNA834827 | ENA |

REPOSITORIES: ENA

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Inhibition of DYRK1A promotes cardiomyocyte proliferation and heart repair after myocardial infarction [RNA-Seq]

Project description:Inhibition of DYRK1A promotes cardiomyocyte proliferation and heart repair after myocardial infarction [RNA-Seq]

| PRJNA834831 | ENA

Inhibition of DYRK1A, via histone modification, promotes cardiomyocyte proliferation and heart repair after myocardial infarction [ChIP-Seq]

Project description:Inhibition of DYRK1A, via histone modification, promotes cardiomyocyte proliferation and heart repair after myocardial infarction [ChIP-Seq]

| PRJNA834830 | ENA

Inhibition of DYRK1A promotes cardiomyocyte proliferation and heart repair after myocardial infarction [RNA-Seq]

Project description:To explore effect of DYRK1A silencing on gene expression of primary cultured cardiomyocytes isolated from 1-day-old SD rats

2022-05-06 | GSE202169 | GEO

Inhibition of DYRK1A, via histone modification, promotes cardiomyocyte proliferation and heart repair after myocardial infarction [ChIP-Seq]

Project description:To explore effect of DYRK1A silencing on H3K4me3 and H3K27ac modification of primary cultured cardiomyocytes isolated from 1-day-old SD rats

2022-05-06 | GSE202168 | GEO

Inhibition of DYRK1A promotes cardiomyocyte proliferation and heart repair after myocardial infarction

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-05-06 | GSE202170 | GEO

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

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Transferrin improved the generation of cardiomyocyte from human pluripotent stem cells for myocardial infarction repair

Project description:Transferrin improved the generation of cardiomyocyte from human pluripotent stem cells for myocardial infarction repair

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Targeting cardiomyocyte ADAM10 ectodomain shedding promotes survival early after myocardial infarction

Project description:Myocardial infarction (MI) contributes to cardiac mortality and morbidity. After myocardial infarction the innate immune response is pivotal in clearing of tissue debris as well as scar formation, but exaggerated cytokine and chemokine secretion with subsequent leukocyte infiltration also leads to further tissue damage. Post-translational regulation of cytokine / chemokine signaling occurs via ectodomain shedding through a disintegrin and metalloproteases (ADAMs). Here, we address the value of targeting a previously unknown ADAM10 / CX3CL1 axis in the regulation of neutrophil recruitment early after MI. We show that myocardial ADAM10 is distinctly upregulated in biopsies from patients with ischemia-driven cardiomyopathy and correlates with heart failure progression. Intriguingly, upon MI in mice, pharmacological treatment with the ADAM10 inhibitionor GI254023X as well as genetic cardiomycyte-specific ADAM10 deletion improves survival with markedly enhanced heart function and reduced scar size. Mechanistically, this is driven by abolished ADAM10-mediated CX3CL1 ectodomain shedding followed by diminished IL-1β-dependent inflammation, reduced neutrophil bone marrow egress as well as myocardial tissue infiltration. Genetic cardiomycyte-specific ADAM10 deletion confirmes the small-molecule data and leads to improved cardiac function and reduction in inflammatory markers after ischemic myocardial injury. Thus, our data shows a conceptual insight into how acute MI induces chemotactic signaling via ectodomain shedding in cardiomyocytes.

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Spatial multi-omic map of human myocardial infarction

Project description:Myocardial infarction is a leading cause of mortality worldwide 1 . While advances have been made in acute treatment, an incomplete understanding of remodelling processes has limited the effectiveness of therapies to reduce late-stage mortality 2 . Here, we generate an integrative high- resolution map of human cardiac remodelling after myocardial infarction using single-cell gene expression, chromatin accessibility, and spatial transcriptomic profiling of multiple physiological zones at distinct time points in myocardium from myocardial infarction and control patients. Multimodal data integration allowed us to evaluate cardiac cell-type compositions at increased resolution, yielding insights into changes of the cardiac transcriptome and epigenome through the identification of distinct tissue structures of injury, repair and remodelling. We identified and validated disease-specific cardiac cell-states of major cell-types and analysed them in their spatial context, evaluating their dependency on other cell-types. Our data elucidates molecular principles of human myocardial tissue organisation, recapitulating a gradual cardiomyocyte and myeloid continuum following ischemic injury. In total, our study provides an integrative molecular map of human myocardial infarction and represents an essential reference for the field and paves the way for advanced mechanistic and therapeutic studies of cardiac disease.

| EGAS00001006330 | EGA

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