Lipoxin A4 depresses inflammation and promotes autophagy via AhR/mTOR/AKT pathway to suppress endometriosis

Zhixiong Huang, Huang ZX, Zhi-Xiong Huang, Xiao-Rong He, Xiaorong He, He XR, Xin-Yu Ding, Ding XY, Xinyu Ding, Jiahao Chen, Chen JH, Jia-Hao Chen, Yi‐Hong Lei, Yi-Hong Lei, Lei YH, Bai JB, Jian-Bing Bai, Jian‐Bing Bai, Dianchao Lin, Lin DC, Dian-Chao Lin, Hong YH, Yi-Huang Hong, Yi‐Huang Hong, Jianfa Lan, Lan JF, Jian-Fa Lan, Qionghua Chen
American journal of reproductive immunology (New York, N.Y. : 1989) · 2022 · vol. 89(3) , pp. e13659 · doi:10.1111/aji.13659 · PMID:36412044 · W4309655221
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Lipoxin A4 suppresses endometriosis by reducing inflammation and promoting autophagy through the AhR/mTOR/AKT pathway.

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Abstract

BACKGROUND: Endometriosis is a benign gynecological disease with the feature of estrogen dependence and inflammation. The function of autophagy and the correlation with inflammation were not yet revealed. METHODS: Autophagosomes were detected by transmission electron microscopy. Gene Expression Omnibus (GEO) database was referred to analyze the expression of autophagy-related genes. Quantification of mRNA and protein expression was examined by qRT-PCR and Western Blot. Immunohistochemistry was performed to explore the expression of proteins in tissues. The mouse model of endometriosis was performed to analyze the autophagic activity and effect of LXA4. RESULTS: The expression of autophagy-related genes in endometriotic lesions were unusually changed. The number of autophagosomes and LC3B-II expression was diminished, and p62 was increased in ectopic lesions from both patients and mice. Interleukin 1β (IL1β) attenuated the expression of LC3B and promoted the level p62. The autophagy activator MG-132 upregulated the expression of LC3B and reduced IL1β, IL6, and p62. LXA4 reversed the inhibitory effect of IL1β on the expression of LC3B and p62, and blocking the receptor of LXA4 AhR (aryl hydrocarbon receptor) resulted in the incapacitation of LXA4 to influence the effect of IL1β. LXA4 depressed the phosphorylation of AKT and mTOR to against IL1β, and blocking AhR negatively regulated the effect of LXA4 on AKT/mTOR pathway. LXA4 reduced the ectopic lesions and the expression of IL1β and p62, but enhanced LC3B-II in endometriotic mouse models. CONCLUSION: In endometriosis, increased inflammation of ectopic lesions prominently depresses autophagy. LXA4 could regulate autophagy by suppressing inflammatory response through AhR/AKT/mTOR pathway.

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Condition tags

endometriosis

MeSH descriptors

Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis

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Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. [ expand to 2 hops ] — adds papers reached through this work's immediate citers/citees. Heavier; up to 60 extra dots.

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