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The m6A methyltransferase Mettl3 deficiency attenuates hepatic stellate cell activation and liver fibrosis

ABSTRACT: The m6A methyltransferase Mettl3 deficiency attenuates hepatic stellate cell activation and liver fibrosis

PROVIDER: PRJNA857659 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR20077400_1.fastq.gz	Fastqsanger.gz
	SRR20077400_2.fastq.gz	Fastqsanger.gz
	SRR20077386_1.fastq.gz	Fastqsanger.gz
	SRR20077386_2.fastq.gz	Fastqsanger.gz
	SRR20077387_1.fastq.gz	Fastqsanger.gz

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The m6A methyltransferase Mettl3 deficiency attenuates hepatic stellate cell activation and liver fibrosis [m6A-RIP-seq]

Project description:m6A-RIP sequencing of primary hepatic stellate cells (HSCs) isolated from Control and HSC-specific Mettl3-knockout (Mettl3 cKO) mouse liver tissues.

2022-07-13 | GSE207908 | GEO

The m6A methyltransferase Mettl3 deficiency attenuates hepatic stellate cell activation and liver fibrosis [RNA-seq]

Project description:RNA sequencing of LX2 cell line (a human hepatic stellate cell line). METTL3 overexpression or downreguation were achieved by lenti-virus transduction.

2022-07-13 | GSE207909 | GEO

The m6A methyltransferase Mettl3 deficiency attenuates hepatic stellate cell activation and liver fibrosis [m6A-RIP-seq]

Project description:The m6A methyltransferase Mettl3 deficiency attenuates hepatic stellate cell activation and liver fibrosis [m6A-RIP-seq]

| PRJNA857667 | ENA

The m6A methyltransferase Mettl3 deficiency attenuates hepatic stellate cell activation and liver fibrosis [RNA-seq]

Project description:The m6A methyltransferase Mettl3 deficiency attenuates hepatic stellate cell activation and liver fibrosis [RNA-seq]

| PRJNA857666 | ENA

m6A methyltransferase METTL3 regulates Tfh cell differentiation

Project description:m6A methyltransferase METTL3 regulates Tfh cell differentiation

| PRJNA532389 | ENA

The m6A methyltransferase Mettl3 deficiency attenuates hepatic stellate cell activation and liver fibrosis

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-07-13 | GSE207910 | GEO

Mettl3-dependent m6A modulation of mRNAs in the Drosophila brain attenuates the stress response

Project description:We observe the increase of stress resilience in Drosophila in which the m6A methyltransferase Mettl3 is knocked down. Mettl3-dependent m6A is present in the 5' UTR of genes enriched for neurogenesis and signaling pathways, and determine that Mettl3-dependent m6A regulates the decay of heat shock chaperones. Expression levels of genes with Mettl3-dependent m6A are increased with the reduction of Mettl3 and with heat shock stress in the brain.

2022-08-26 | GSE178955 | GEO

Exploring the Impact of m6A Methyltransferase Mettl3 on MASLD through Multi-Omics Analysis

Project description:Background: N6-methyladenosine (m6A) RNA modification plays a crucial role in various biological events and is implicated in various metabolic-related diseases. However, its role in MASLD remains unclear. This study aims to investigate the impact of Mettl3 on MASLD through multi-omics analysis, with a focus on exploring its potential mechanisms of action. Methods: MASLD mouse models were established by feeding a high-fat diet for 12 weeks, and Mettl3 stable overexpression AML12 cell models were constructed via lentiviral transfection. Subsequent transcriptomic and proteomic analyses, as well as integrated analysis between different omics datasets, were conducted. Results: Mettl3 expression significantly increased in MASLD mouse models. In the transcriptomic and proteomic analyses, we identified 848 genes with significant inconsistencies between transcriptomic and proteomic datasets. GO/KEGG enrichment terms may involve post-transcriptional modifications, particularly Mettl3-mediated m6A modification. Subsequently, through integrated proteomic analysis of Mettl3-overexpressed AML12 cell models and MASLD mouse models, we selected the top 20 co-upregulated and co-downregulated GO/KEGG terms as the main biological processes influenced by Mettl3 in MASLD. By intersecting with pathways obtained from previous integrated analyses, we identified GO/KEGG terms affected by Mettl3-induced m6A modification. Protein-protein interaction analysis of proteins involved in these pathways highlighted GAPDH, ENO1, and TPI1 as three key hub genes. Conclusion: In MASLD, Mettl3 regulates the glycolytic pathway through m6A modification, influencing the occurrence and development of the disease via the key hub genes GAPDH, ENO1, and TPI1. These findings expand our understanding of MASLD and provide strong evidence for potential therapeutic targets and drug development.

2024-09-20 | PXD050565 | Pride

Determine the methyltransferase activities of METTL3, METTL14, and METTL16 via MeRIP-seq (m6A-seq)

Project description:All the three enzymes, METTL3, METTL14, and METTL16, belong to methyltransferase like (METTL) family and possess the ability to deposit N6-methyladenosine (m6A) in mRNA. Via immunofluorescence staining and wertern blotting, we discovered either METTL3 or METTL14 mainly localize in nuclear, but METTL16 localizes in both cytosol and nuclei. To compare the m6A methyltransferase activities of the three m6A 'writers' and better understand their differences, MeRIP-seq (m6A-seq) was conducted with poly(A) RNAs isolaed from HEK293T cells with METTL3, 14 and 16 knockout.

2021-10-28 | GSE182607 | GEO

The m<sup>6</sup>A methyltransferase Mettl3 deficiency attenuates hepatic stellate cell activation and liver fibrosis.

Project description:Activation of hepatic stellate cells (HSCs) is a central driver of liver fibrosis. Previous investigations have identified various altered epigenetic landscapes during the cellular progression of HSC activation. N6-methyladenosine (m6A) is the most abundant internal RNA modification in eukaryotic cells and is dynamically regulated under various physiological and pathophysiological conditions. However, the functional role of Mettl3-mediated m6A in liver fibrosis remains elusive. Here, we found that the HSC-specific knockout of m6A methyltransferase Mettl3 suppressed HSC activation and significantly alleviated liver fibrosis. Multi-omics analysis of HSCs showed that Mettl3 depletion reduced m6A deposition on mRNA transcripts of Lats2 (a central player of the Hippo/YAP signaling pathway) and slowed down their degradation. Elevated Lats2 increased phosphorylation of the downstream transcription factor YAP, suppressed YAP nuclear translocation, and decreased pro-fibrotic gene expression. Overexpressing YAP mutant resistant to phosphorylation by Lats2 partially rescued the activation and pro-fibrotic gene expression of Mettl3-deficient HSCs. Our study revealed that disruption of Mettl3 in HSCs mitigated liver fibrosis by controlling the Hippo/YAP signaling pathway, providing potential therapeutic strategies to alleviate liver fibrosis by targeting epitranscriptomic machinery.

| S-EPMC9734030 | biostudies-literature

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