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RNA m6A methylation modulates airway inflammation in allergic asthma via PTX3-dependent macrophage homeostasis
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RNA m6A methylation modulates airway inflammation in allergic asthma via PTX3-dependent macrophage homeostasis
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RNA m6A methylation modulates airway inflammation in allergic asthma via PTX3-dependent macrophage homeostasis
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Journal Article
RNA m6A methylation modulates airway inflammation in allergic asthma via PTX3-dependent macrophage homeostasis
2023
Overview
N
6
-methyladenosine (m
6
A), the most prevalent mRNA modification, has an important function in diverse biological processes. However, the involvement of m
6
A in allergic asthma and macrophage homeostasis remains largely unknown. Here we show that m
6
A 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, m
6
A-sequencing shows that loss of
METTL3
impairs the m
6
A-YTHDF3-dependent degradation of
PTX3
mRNA, while higher PTX3 expression positively correlates with asthma severity through promoting M2 macrophage activation. Furthermore, the METTL3/YTHDF3-m
6
A/PTX3 interactions contribute to autophagy maturation in macrophages by modulating
STX17
expression. Collectively, this study highlights the function of m
6
A in regulating macrophage homeostasis and identifies potential targets in controlling allergic asthma.
The function of METTL3 and RNA methylation is important in various biological processes. Here the authors show that METTL3 is reduced in childhood asthma patients and that conditional knockout of Mettl3 in mouse myeloid cells enhances Th2 response and allergic asthma associated with changes in macrophage function.
