Methyltransferase-like 3 (METTL3) Epigenetically Modulates Glutathione Peroxidase 4 (GPX4) Expression to Affect Asthma

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Lin Liangfeng; Hu Xiaohao; Li Qiaoyu; Huang Linlin

مرکز اطلاعات علمی Scientific Information Database (SID) - Trusted Source for Research and Academic Resources

Journal Paper

Paper Information

Journal: Iranian Journal of Allergy, Asthma and Immunology Year:2023 | Volume:22 | Issue:6 Page(s): 551-560

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Title

Methyltransferase-like 3 (METTL3) Epigenetically Modulates Glutathione Peroxidase 4 (GPX4) Expression to Affect Asthma

Author(s)

Lin Liangfeng | Hu Xiaohao | Li Qiaoyu | Huang Linlin | Issue Writer Certificate

Keywords

Asthma

Bronchial disease

Epithelial cells

Ferroptosis

Glutathione peroxidase 4

METTL3 protein

human

Oxidative stress

RNA stability

Abstract

Asthma, a prevalent chronic airway inflammatory condition, poses a significant health challenge. In this study, we delved into the regulatory mechanisms governing Asthma, focusing on Methyltransferase-like 3 (METTL3). Through an ovalbumin (OVA)-induced mouse model and interleukin-13 (IL-13)-induced cell model, we mimicked the in vivo and in vitro functions of METTL3 in Asthma. Our research revealed that METTL3 expression significantly decreased in Asthma-induced mice and IL-13-stimulated cells compared to the control group. Moreover, METTL3 overexpression enhanced bronchial epithelial cell viability and proliferation. Mechanistically, we observed elevated levels of total iron, Fe2+, malondialdehyde (MDA), lipid reactive oxygen species (ROS), alongside reduced glutathione (GSH) levels in IL-13-stimulated cells. Remarkably, METTL3 overexpression counteracted these effects, suggesting a pivotal role in mitigating Asthma-related Oxidative stress. Furthermore, our study highlighted the involvement of N6-methyladenosine methylation (m6A) modification, where METTL3 regulated the m6A modification of Glutathione peroxidase 4 (GPX4) RNA, impacting RNA stability. Knockdown of METTL3 suppressed m6A modification on GPX4 RNA, impairing its stability and contributing to IL-13-induced Ferroptosis. Interestingly, METTL3 overexpression not only inhibited cell Ferroptosis but also alleviated Asthma symptoms. Our findings shed light on the epigenetic regulation of Asthma through METTL3-mediated m6A modification, offering potential therapeutic avenues for this prevalent inflammatory disease.

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