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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

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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]

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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

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

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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.

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

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

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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.

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