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. 2022 May 25;13:897487. doi: 10.3389/fimmu.2022.897487

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Copyright © 2022 Chen, Wu, Zhu, Chen, Xu, Tang, Jiao and Yu

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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METTL3 inhibits endothelial injury in sepsis-induced ARDS through Trim59-associated NF-κB inactivation. (A, C) Immunoblot showing p65 and IκB phosphorylation in HULEC-5a cells treated with or without METTL3 overexpression (A) and METTL3-overexpressing HULEC-5a cells with or without Trim59 siRNA (C). (B) RT-qPCR analysis showing inflammatory cytokine and endothelial functional marker mRNA expression in METTL3-overexpressing HULEC-5a cells treated with or without the NF-κB inhibitor BAY. All data are expressed as the mean ± SD of three independent experiments. *p < 0.05; **p < 0.01; ****p < 0.0001.