AI Article Synopsis
- N-methyladenosine (mA) is a common mRNA modification that plays a key role in various biological processes, but its role in allergic asthma and macrophage function is not well understood.* -
- The study finds that low levels of METTL3, the enzyme that adds mA, in macrophages from childhood asthma patients lead to increased Th2 responses and worse allergic inflammation due to enhanced M2 macrophage activation.* -
- METTL3's regulation of M2 macrophage activation involves specific signaling pathways and affects PTX3 mRNA stability, linking mA modification to macrophage function and potential new avenues for asthma treatment.*
Article Abstract
N-methyladenosine (mA), the most prevalent mRNA modification, has an important function in diverse biological processes. However, the involvement of mA in allergic asthma and macrophage homeostasis remains largely unknown. Here we show that mA methyltransferases METTL3 is expressed at a low level in monocyte-derived macrophages from childhood allergic asthma patients. Conditional knockout of Mettl3 in myeloid cells enhances Th2 cell response and aggravates allergic airway inflammation by facilitating M2 macrophage activation. Loss and gain functional studies confirm that METTL3 suppresses M2 macrophage activation partly through PI3K/AKT and JAK/STAT6 signaling. Mechanistically, mA-sequencing shows that loss of METTL3 impairs the mA-YTHDF3-dependent degradation of PTX3 mRNA, while higher PTX3 expression positively correlates with asthma severity through promoting M2 macrophage activation. Furthermore, the METTL3/YTHDF3-mA/PTX3 interactions contribute to autophagy maturation in macrophages by modulating STX17 expression. Collectively, this study highlights the function of mA in regulating macrophage homeostasis and identifies potential targets in controlling allergic asthma.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10643624 | PMC |
| http://dx.doi.org/10.1038/s41467-023-43219-w | DOI Listing |
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