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METTL3 mediated m6A mRNA methylation regulates neutrophil activation through targeting TLR4 signaling

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE225143 | GEO | 2023/03/31

REPOSITORIES: GEO

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METTL3 mediated m6A mRNA methylation regulates neutrophil activation through targeting TLR4 signaling (Ribosome-Seq)

Project description:To investigate the effect of METTL3 function in the regulation of neutrophil activation, we established neutrophil METTL3 knock out mice by crossing METTL3flox/flox mice with Lyzm-cre mice. We then performed gene expression profiling analysis using data obtained from Ribosome-seq of isolated neutrophil from METTL3f/f and METTL3f/f Lyzm-Cre mice .

2023-03-31 | GSE225140 | GEO

METTL3 mediated m6A mRNA methylation regulates neutrophil activation through targeting TLR4 signaling (RNA-Seq)

Project description:To investigate the effect of METTL3 function in the regulation of neutrophil activation, we established neutrophil METTL3 knock out mice by crossing METTL3flox/flox mice with Lyzm-cre mice. We then performed gene expression profiling analysis using data obtained from RNA-seq of isolated neutrophil from METTL3f/f and METTL3f/f Lyzm-Cre mice with or without intraperitoneal injection of lipopolysaccharide (LPS) treatment.

2023-03-31 | GSE225141 | GEO

METTL3 mediated m6A mRNA methylation regulates neutrophil activation through targeting TLR4 signaling (meRIP-Seq)

Project description:To investigate the effect of METTL3 function in the regulation of neutrophil activation, we established neutrophil METTL3 knock out mice by crossing METTL3flox/flox mice with Lyzm-cre mice. We then performed gene expression profiling analysis using data obtained from MeRIP-seq of isolated neutrophil from METTL3f/f and METTL3f/f Lyzm-Cre mice .

2023-03-31 | GSE225139 | GEO

METTL3 mediated m6A mRNA methylation regulates neutrophil activation through targeting TLR4 signaling

Project description:METTL3 mediated m6A mRNA methylation regulates neutrophil activation through targeting TLR4 signaling

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METTL3 mediated m6A mRNA methylation regulates neutrophil activation through targeting TLR4 signaling (meRIP-Seq)

Project description:METTL3 mediated m6A mRNA methylation regulates neutrophil activation through targeting TLR4 signaling (meRIP-Seq)

| PRJNA934077 | ENA

METTL3 mediated m6A mRNA methylation regulates neutrophil activation through targeting TLR4 signaling (RNA-Seq)

Project description:METTL3 mediated m6A mRNA methylation regulates neutrophil activation through targeting TLR4 signaling (RNA-Seq)

| PRJNA934079 | ENA

METTL3 mediated m6A mRNA methylation regulates neutrophil activation through targeting TLR4 signaling (Ribosome-Seq)

Project description:METTL3 mediated m6A mRNA methylation regulates neutrophil activation through targeting TLR4 signaling (Ribosome-Seq)

| PRJNA934078 | ENA

CMTM3 regulates neutrophil activation and aggravates sepsis through TLR4 signaling

Project description:Regulation of neutrophil activation plays a significant role in managing sepsis. CKLF-like MARVEL transmembrane domain containing (CMTM)3 is a membrane protein involved in immune response. Here, we find that CMTM3 expression is elevated in sepsis and plays a crucial role in mediating the imbalance of neutrophil migration. Cmtm3 knockout improves the survival rate of septic mice, mitigate inflammatory responses, and ameliorate organ damage. Mechanistically, the deletion of Cmtm3 reduced the expression of Toll-like receptor 4 (TLR4) on neutrophils, leading to a decrease in the expression of C-X-C motif chemokine receptor 2 (CXCR2) on the cell membrane. This resulted in a reduced migration of neutrophils from the bone marrow to the bloodstream, thereby attenuating their recruitment to vital organs. Our findings suggest that targeting CMTM3 holds promise as a therapeutic approach to ameliorate the dysregulation of neutrophil migration and multi-organ damage associated with sepsis.

| S-SCDT-10_1038-S44319-024-00291-7 | biostudies-other

Mettl3-mediated m6A regulates spermatogonial differentiation and meiosis initiation.

Project description:METTL3 catalyzes the formation of N6-methyl-adenosine (m6A) which has important roles in regulating various biological processes. However, the in vivo function of Mettl3 remains largely unknown in mammals. Here we generated germ cell-specific Mettl3 knockout mice and demonstrated that Mettl3 was essential for male fertility and spermatogenesis. The ablation of Mettl3 in germ cells severely inhibited spermatogonial differentiation and blocked the initiation of meiosis. Transcriptome and m6A profiling analysis revealed that genes functioning in spermatogenesis had altered profiles of expression and alternative splicing. Our findings provide novel insights into the function and regulatory mechanisms of Mettl3-mediated m6A modification in spermatogenesis and reproduction in mammals.

| S-EPMC5587845 | biostudies-literature

piRNA-36741 regulates BMP2-mediated osteoblast differentiation via METTL3 controlled m6A modification.

Project description:The osteogenic differentiation of bone marrow mesenchymal stem cells (BMSCs) is essential for bone formation, and its imbalance can lead to bone diseases such as osteoporosis. It is reported that PIWI-interacting RNA-36741 (piR-36741) is up-regulated during the osteogenic differentiation, but its role in regulating osteogenic differentiation remains unclear. Here, the primary human BMSCs were used to induce osteogenic differentiation, and the expression of piR-36741 and METTL3 (methyltransferase like 3) was up-regulated during the osteogenic differentiation of BMSCs. Moreover, interference with piR-36741 or METTL3 markedly hindered the osteogenic differentiation of BMSCs, which was manifested by a reduction in osteoblast marker expression (including RUNX2, COL1A1, OPN and OCN), osteogenic phenotype and matrix mineralization. Mechanistically, the piR-36741-PIWIL4 complex directly interacted with METTL3 and prevented METTL3-mediated m6A modification of BMP2 mRNA transcripts, thereby promoting BMP2 expression. And overexpression of BMP2 reversed the inhibitory effect of piR-36741 silence on osteogenic differentiation and the Smad pathway activity. In addition, administration with piR-36741 mimic alleviated ovariectomy-induced osteoporosis in mice. In conclusion, piRNA-36741 overexpression promoted osteogenic differentiation of BMSCs and mitigated ovariectomy-induced osteoporosis through METTL3-mediated m6A methylation of BMP2 transcripts.

| S-EPMC8544320 | biostudies-literature

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