Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

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

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

PROVIDER: PRJNA421012 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR6345651.fastq.gz	Fastqsanger.gz
	SRR6345652.fastq.gz	Fastqsanger.gz
	SRR6345653.fastq.gz	Fastqsanger.gz
	SRR6345654.fastq.gz	Fastqsanger.gz

Items per page:

1 - 4 of 4

Similar Datasets

Loss of microRNA-128 promotes cardiomyocyte proliferation and heart regeneration

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

| PRJNA421019 | ENA

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

Project description:To identify the potential microRNAs (miRNAs) involved in the regulation of cardiomyocyte (CM) proliferation during homeostasis and injury, RNA sequencing (RNA-seq) in mouse cardiac ventricles was performed on postnatal day 1, 7, and 28 (P1, P7, and P28). Significant upregulation of MiR-128 was found in P7 hearts as compared to P1. To further specify the effect of miR-128 in the heart, RNA-Seq was performed in control mice (Ctrl) and miR-128 overexpression mice (miR-128OE) on P7. These data provide novel insights into the mechanisms by which adult CMs exit the cell cycle arrest and is fundamental for therapeutic manipulation to stimulate endogenous CM proliferate in cardiac regeneration.

2018-01-02 | GSE107679 | GEO

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

2018-01-02 | GSE107678 | GEO

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

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

| PRJNA421014 | ENA

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.

2025-02-13 | MTBLS12191 | MetaboLights

Gas6 promotes Cardiomyocyte Proliferation and Heart Regeneration

Project description:Gas6 promotes Cardiomyocyte Proliferation and Heart Regeneration

| PRJNA1309049 | ENA

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

Project description: Not available

| S-EPMC5816015 | biostudies-literature

Gas6 promotes Cardiomyocyte Proliferation and Heart Regeneration

Project description:Ischemic heart disease remains a leading cause of mortality, with limited adult cardiac regeneration due to insufficient cardiomyocyte proliferation. This study investigates the role of Growth Arrest-Specific Gene 6 (Gas6) in regulating cardiomyocyte cell cycle and promoting cardiac repair. Gas6 expression declines postnatally in cardiomyocytes but increases during neonatal heart regeneration following myocardial infarction (MI). Cardiomyocyte-specific Gas6 knockout (Gas6CKO) mice exhibited reduced cardiomyocyte proliferation, decreased total cardiomyocyte numbers, and delayed-onset heart failure with ventricular dilation by ~250 days, as confirmed by transcriptomic analysis revealing downregulation of cell cycle pathways and upregulation of fibrotic and contractile genes in Gas6CKO versus control hearts at 250 days. Conversely, AAV9-mediated cardiomyocyte-specific Gas6 overexpression enhanced neonatal cardiomyocyte proliferation, dedifferentiation, and hyperplastic growth, while in adult MI models, it improved cardiac function, reduced infarct size, and increased proliferative markers (Ki67, pH3, Aurora B) in the border zone. Bulk RNA-sequencing of primary mouse cardiomyocytes overexpressing Ad-Gas6 versus controls identified upregulated cell cycle and mitotic pathways, alongside downregulated cardiac contraction and extracellular matrix organization, with transcription factor enrichment highlighting Yap-mediated activation via TEAD2 and E2F1. Mechanistically, Gas6 binds Sav1 to disrupt the Sav1-Mst1 complex, inhibiting Hippo pathway phosphorylation, promoting Yap nuclear translocation, and driving cell cycle gene expression. These findings position Gas6 as a therapeutic target for cardiac regeneration in ischemic heart disease.

2026-08-21 | GSE306068 | GEO

Tp53 suppression promotes cardiomyocyte proliferation during zebrafish heart regeneration

Project description:Tp53 suppression promotes cardiomyocyte proliferation during zebrafish heart regeneration

| PRJNA612190 | ENA

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.

2026-05-01 | GSE302427 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data