Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Remodeling of the m6A landscape in the heart reveals conserved post-transcriptional events underlying cardiomyocyte hypertrophy

ABSTRACT: Remodeling of the m6A landscape in the heart reveals conserved post-transcriptional events underlying cardiomyocyte hypertrophy

PROVIDER: PRJNA668129 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR12795900.fastq.gz	Fastqsanger.gz
	SRR12795901.fastq.gz	Fastqsanger.gz
	SRR12795902.fastq.gz	Fastqsanger.gz
	SRR12795903.fastq.gz	Fastqsanger.gz
	SRR12795904.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 20

Similar Datasets

Remodeling of the m6A landscape in the heart reveals conserved post-transcriptional events underlying cardiomyocyte hypertrophy

Project description:Regulation of gene expression plays a fundamental role in cardiac stress-responses. Modification of coding transcripts by adenosine methylation (m6A) has recently emerged as a critical post-transcriptional mechanism underlying heart disease. Thousands of mammalian mRNAs are known to be m6A-modified, suggesting that remodeling of the m6A landscape may play an important role in cardiac pathophysiology. Here we found an increase in m6A content in human heart failure samples. We then adopted genome-wide analysis to define all m6A-regulated sites in human failing compared to non-failing hearts and identified targeted transcripts involved in histone modification as enriched in heart failure. Further, we compared all m6A sites regulated in human hearts with the ones occurring in isolated rat hypertrophic cardiomyocytes to define cardiomyocyte-specific m6A events conserved across species. Our results identified 38 shared transcripts targeted by m6A during stress conditions, and 11 events that are unique to unstressed cardiomyocytes. Of these, Coronin-6 (CORO6) was further evaluated for mRNA and protein abundances, demonstrating the potential impact of m6A on post-transcriptional regulation of gene expression in the heart.

2020-11-01 | GSE159243 | GEO

G3bp1-miR-1 axis regulates cardiomyocyte hypertrophy

Project description:G3bp1-miR-1 axis regulates cardiomyocyte hypertrophy

| PRJNA764679 | ENA

Cardiomyocyte Transcriptomes in Cardiac Development and Hypertrophy

Project description:Cardiomyocyte Transcriptomes in Cardiac Development and Hypertrophy

| PRJNA530023 | ENA

Cardiomyocyte gene programs encoding morphological and functional signatures in cardiac hypertrophy and failure (RNA-Seq)

Project description:Pressure overload induces a transition from cardiac hypertrophy to heart failure, but its underlying mechanisms remain elusive. Here we reconstruct a trajectory of cardiomyocyte remodeling and clarify distinct cardiomyocyte gene programs encoding morphological and functional signatures in cardiac hypertrophy and failure, by integrating single-cardiomyocyte transcriptome with cell morphology, epigenomic state and heart function. During early hypertrophy, cardiomyocytes activate mitochondrial translation/metabolism genes, whose expression is correlated with cell size and linked to ERK1/2 and NRF1/2 transcriptional networks. Persistent overload leads to a bifurcation into adaptive and failing cardiomyocytes, and p53 signaling is specifically activated in late hypertrophy. Cardiomyocyte-specific p53 deletion shows that cardiomyocyte remodeling is initiated by p53-independent mitochondrial activation and morphological hypertrophy, followed by p53-dependent mitochondrial inhibition, morphological elongation, and heart failure gene program activation. Human single-cardiomyocyte analysis validates the conservation of the pathogenic transcriptional signatures. Collectively, cardiomyocyte identity is encoded in transcriptional programs that orchestrate morphological and functional phenotypes.

2018-07-30 | GSE95140 | GEO

Cardiomyocyte gene programs encoding morphological and functional signatures in cardiac hypertrophy and failure (ChIP-Seq)

2018-07-30 | GSE95142 | GEO

Circular RNA circZFPM2 regulates cardiomyocyte hypertrophy and survival

Project description:Circular RNA circZFPM2 regulates cardiomyocyte hypertrophy and survival

| PRJNA1085328 | ENA

Downstream targets of uc.323-mediated cardiomyocyte hypertrophy

Project description:Downstream targets of uc.323-mediated cardiomyocyte hypertrophy

| PRJNA592523 | ENA

Circular RNA circZFPM2 regulates cardiomyocyte hypertrophy and survival

Project description:Hypertrophic cardiomyopathy (HCM) constitutes the most common genetic cardiac disorder. However, current pharmacotherapeutics are mainly symptomatic and only partially address underlying molecular mechanisms. Circular RNAs (circRNAs) are a recently discovered class of non-coding RNAs and emerged as specific and powerful regulators of cellular functions. By performing global circRNA-specific next generation sequencing in cardiac tissue of patients with hypertrophic cardiomyopathy compared to healthy donors, we identified circZFPM2 (hsa_circ_0003380. CircZFPM2, which derives from the ZFPM2 locus, is a highly conserved regulatory circRNA that is strongly induced in HCM tissue. In vitro loss-of-function experiments were performed in neonatal rat cardiomyocytes, human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs), and HCM-patient-derived hiPSC-CMs. A knockdown of circZFPM2 was found to induce cardiomyocyte hypertrophy and compromise mitochondrial respiration, leading to an increased production of reactive oxygen species and apoptosis. In contrast, delivery of recombinant circZFPM2, packaged in lipid-nanoparticles or using AAV-based overexpression, rescued cardiomyocyte hypertrophic gene expression and promoted cell survival. Additionally, HCM-derived cardiac organoids exhibited improved contractility upon CM-specific overexpression of circZFPM2. Multi-Omics analysis further promoted our hypothesis, showing beneficial effects of circZFPM2 on cardiac contractility and mitochondrial function. Collectively, our data highlight that circZFPM2 serves as a promising target for the treatment of cardiac hypertrophy including HCM.

2024-04-25 | GSE261129 | GEO

Slc39a2-mediated Zinc Homeostasis Modulates Innate Immune Signaling in Phenylephrine-induced Cardiomyocyte Hypertrophy

Project description:Zinc dyshomeostasis has been involved in the pathogenesis of cardiac hypertrophy; however, the dynamic regulation of intracellular zinc and its downstream signaling in cardiac hypertrophy remain largely unknown. Here we screened ZIP (SLC39) family members that were responsible for zinc uptake in a phenylephrine (PE)-induced cardiomyocyte hypertrophy model. We found that Slc39a2 was the only member that was altered at mRNA level by PE treatment in neonatal rat ventricular myocytes (NRVMs), but its protein level was not affected. Zincpyr1 staining showed a significant decrease in zinc uptake after PE treatment or after Slc39a2 knockdown in NRVMs, indicating an inhibition of its transport activity during hypertrophy. Slc39a2 deficiency caused spontaneous hypertrophy in NRVMs, and further exacerbated the hypertrophic responses after PE treatment. RNA sequencing analysis confirmed a largely aggravated pro-hypertrophic transcriptome reprogramming after Slc39a2 knockdown. Interestingly, the innate immune pathways, including NOD signaling, TOLL-like receptor, NFB, and IRFs, were substantially enriched after Slc39a2 knockdown. Whereas IRF7, the most sensitive among all IRFs, did not mediate the effect of Slc39a2 in hypertrophy, pro-hypertrophy phosphorylations of NFB and STAT3 were significantly enhanced after Slc39a2 knockdown, in parallel with degradation of IkBα protein. Our data demonstrate that SLC39A2-mediated zinc homeostasis contributes to the remodeling of innate immune signaling in cardiomyocyte hypertrophy, and provide novel insights into the pathogenesis of heart failure and its treatment.

2021-11-24 | GSE175884 | GEO

NAP1L5 is required for translation activation during cardiomyocyte hypertrophy

Project description:NAP1L5 is required for translation activation during cardiomyocyte hypertrophy

| PRJNA770527 | ENA