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

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

PROVIDER: PRJNA834831 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19621846_1.fastq.gz	Fastqsanger.gz
	SRR19621846_2.fastq.gz	Fastqsanger.gz
	SRR19621847_1.fastq.gz	Fastqsanger.gz
	SRR19621847_2.fastq.gz	Fastqsanger.gz
	SRR19621848_1.fastq.gz	Fastqsanger.gz

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

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

| PRJNA834827 | 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

α-Ketoglutarate Promotes Cardiomyocyte Proliferation and Heart Regeneration after Myocardial Infarction

Project description:The neonatal mammalian heart is capable of substantial regeneration following injury through cardiomyocyte proliferation. However, this regenerative capacity is lost by postnatal (P) day 7. How to stimulate the adult cardiomyocyte to re-enter the cell cycle is still unknown. Accumulating evidence suggests that cardiomyocyte proliferation depends on its metabolic state. Due to the tight connection between the tricarboxylic acid cycle (TCA) and cell proliferation, we analyzed the TCA metabolites between P0.5 and P7 mouse hearts and found that α-ketoglutarate (α-KG) ranked first among the decreased metabolites. The intraperitoneal injection of exogenous α-KG extended the window of cardiomyocyte proliferation during heart development and promoted heart regeneration after myocardial infarction (MI) by inducing adult cardiomyocyte proliferation. This was confirmed in Ogdh-siRNA-treated mice with increased α-KG levels. Mechanistically, α-KG activates Jmjd3, a histone lysine demethylase, that decreases H3K27me3 expression and deposition of H3K4me3 at the promoters of cell cycle and structural maturation genes in cardiomyocytes. Our present study shows that α-KG promotes cardiomyocyte proliferation by Jmjd3-dependent demethylation and inactivation of H3K27me3 andH3K4me3, which is a potential therapeutic approach for treating MI and heart failure.

2024-07-12 | GSE272104 | 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

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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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

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.

2022-11-10 | GSE217268 | GEO

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