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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

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			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

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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.

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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.

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