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Loss of microRNA-128 promotes cardiomyocyte proliferation and heart regeneration [miRNA-seq]

ABSTRACT: Loss of microRNA-128 promotes cardiomyocyte proliferation and heart regeneration [miRNA-seq]

PROVIDER: PRJNA421014 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6345661.fastq.gz	Fastqsanger.gz
	SRR6345662.fastq.gz	Fastqsanger.gz
	SRR6345663.fastq.gz	Fastqsanger.gz

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Loss of microRNA-128 promotes cardiomyocyte proliferation and heart regeneration

Project description:Loss of microRNA-128 promotes cardiomyocyte proliferation and heart regeneration

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Loss of microRNA-128 promotes cardiomyocyte proliferation and heart regeneration [miRNA-seq]

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Loss of microRNA-128 promotes cardiomyocyte proliferation and heart regeneration [RNA-seq]

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Loss of microRNA-128 promotes cardiomyocyte proliferation and heart regeneration [RNA-seq]

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FOXK1 and FOXK2 Promote Cardiomyocyte Proliferation and Heart Regeneration

Project description:Promoting the proliferation of endogenous cardiomyocytes represents a promising strategy for treating cardiac injuries. Identifying key factors that regulate cardiomyocyte proliferation can advance the development of novel therapies for heart regeneration. Here we identify that FOXK1 and FOXK2 act as master regulators of cardiomyocyte proliferation and metabolism. The expression of FOXK1 and FOXK2 decreased with postnatal heart development. Cardiomyocyte-specific knockout of Foxk1 or Foxk2 inhibited neonatal heart regeneration after myocardial infarction (MI) injury. Conversely, AAV9-mediated cardiomyocyte-specific overexpression of FOXK1 or FOXK2 prolonged the postnatal proliferative window of cardiomyocytes and enhanced cardiac repair in adult mice by promoting endogenous cardiomyocyte proliferation after MI. Mechanistically, FOXK1 and FOXK2 induce Ccnb1 and Cdk1 transcription and cardiomyocyte cell cycle progression, respectively. Ccnb1 knockdown hindered FOXK1 overexpression-induced cardiomyocyte proliferation, and the same effect was observed when Cdk1 was knocked down in FOXK2 overexpressing cardiomyocytes. Additionally, we further revealed that FOXK1 and FOXK2 induced a metabolic shift toward glycolysis by promoting HIF1α expression in cardiomyocytes, which favors cardiomyocyte proliferation. Our findings identify FOXK1 and FOXK2 as critical triggers of cardiomyocyte proliferation and define these two transcription factors as novel therapeutic targets for myocardial infarction.

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Loss of microRNA-128 promotes cardiomyocyte proliferation and heart regeneration.

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Tp53 suppression promotes cardiomyocyte proliferation during zebrafish heart regeneration

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HMGB2 Promotes Cardiomyocyte Proliferation and Heart Regeneration Through MTA2-driven Metabolic Reprogramming

Project description:Neonatal heart possesses the unique ability to regenerate post-injury. Underlying related mechanisms and reactivation of this process are crucial for regeneration medicine. Using quantitative proteomics with tandem mass tag labeling, RNA-sequencing (RNA-seq) and single-nucleus RNA-seq dataset analyses, high mobility group box 2 (HMGB2) was identified as a key regulator of cardiomyocyte proliferation, whose expression declines during postnatal heart development and increases in the high regenerative potential cardiomyocyte populations in hearts post-injury. Cardiomyocyte-specific HMGB2 knockdown curtails cardiomyocyte proliferation and impairs heart regeneration following apical resection (AR) in neonatal mice, while cardiomyocyte-specific HMGB2 overexpression enhances cardiomyocyte proliferation and facilitates cardiac regeneration and repair in adult mice post-myocardial infarction (MI). Mechanistically, RNA-seq analysis revealed that HMGB2 promotes cardiomyocyte proliferation via activating hypoxia inducible factor 1ɑ (HIF-1α)-mediated glycolysis. This study further found HMGB2 can directly interact with metastasis-associated protein 2 (MTA2) and inhibit its ubiquitination degradation to stabilize HIF-1α protein through immunoprecipitation-mass spectrometry (IP-MS) analysis. Finally, activating HIF-1α or MTA2 could also promote cardiomyocyte proliferation and cardiac repair in adult mice following MI. Taken together, these findings highlight HMGB2 plays a crucial role in promoting heart regeneration through regulating glycolysis. Activating the HMGB2-MTA2-HIF-1α axis might serve as potential therapeutic options for regenerative therapies post-myocardial injury.

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Murine neonatal cardiac B cells promote cardiomyocyte proliferation and heart regeneration

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