Attenuated monoamine oxidase a impairs endometrial receptivity in women with adenomyosis via downregulation of FOXO1

Jiao Tian, Chunxue Zhang, Nannan Kang, Junxia Wang, Na Kong, Jidong Zhou, Min Wu, Lijun Ding, Haixiang Sun, Guijun Yan, Xiaoqiang Sheng
Biology of reproduction · 2021 · vol. 105(6) , pp. 1443–1457 · doi:10.1093/biolre/ioab182 · PMID:34568943 · W3202221521
article OA: closed CC0 ⤵ 4 in-corpus citations
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Attenuated monoamine oxidase A impairs endometrial receptivity in women with adenomyosis by downregulating FOXO1, leading to inappropriate endometrial epithelial cell proliferation.

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Abstract

The establishment of endometrial receptivity is a prerequisite for successful pregnancy. Women with adenomyosis possess a lower chance of clinical pregnancy after assisted reproductive technology, which is partially due to impaired endometrial receptivity. The establishment of endometrial receptivity requires the participation of multiple processes, and proper endometrial epithelial cell (EEC) proliferation is indispensable. Monoamine oxidase A (MAOA) is a key molecule that regulates neurotransmitter metabolism in the nervous system. In the present study, we demonstrated a novel role for MAOA in the establishment of endometrial receptivity in women with adenomyosis and in an adenomyotic mouse model. Attenuated MAOA impairs endometrial receptivity by promoting inappropriate proliferation of EECs via the downregulation of FOXO1 during the window of implantation. These results revealed that MAOA plays a vital role in endometrial receptivity in female reproduction.

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Condition tags

adenomyosis

MeSH descriptors

Adenomyosis Down-Regulation Endometrium Forkhead Box Protein O1 Monoamine Oxidase Adenomyosis Adenomyosis Adult Animals Endometrium Endometrium Female Forkhead Box Protein O1 Humans Mice Mice, Inbred ICR Monoamine Oxidase Monoamine Oxidase Young Adult

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