Hypoxia stimulates CXCR4, an EMT-related factor expression in endometrial epithelial cells

Naoya Tsubata, Kazuya Kusama, Kazuhiro Tamura
In: Proceedings for Annual Meeting of The Japanese Pharmacological Society · 2020 · vol. 93(0) , pp. 1–SS · doi:10.1254/jpssuppl.93.0_1-ss-12 · W3011508733
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Hypoxia increased CXCR4, an EMT marker, in endometrial epithelial cells, and thrombin/PGE2 further enhanced its expression and migration under hypoxic conditions.

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The study examined how hypoxia and inflammatory mediators influence epithelial–mesenchymal transition (EMT) marker expression and migration in human endometrial epithelial cells, using the EM-1 epithelial line and EtsT499 stromal cells in a 3D culture system. Cells were incubated for 18 hours under hypoxia and then treated for 72 hours with thrombin (a PAR agonist) plus PGE2 (PG EP2 pathway mediator), with EMT-related marker expression including CXCR4 assessed. Hypoxia increased CXCR4 expression in EM-1 but not in EtsT499, and thrombin/PGE2 did not alter CXCR4 in either cell; however, thrombin/PGE2 promoted EM-1 migration under hypoxia. The authors specifically connect these findings to endometriosis by proposing that inflammatory mediators in retrograde menstrual fluid may be involved in ectopic endometrial EMT and migration. This paper is centrally about endometriosis — it investigates hypoxia-driven CXCR4/EMT and EMT-associated migration of endometrial epithelial cells in a framework relevant to ectopic growth in endometriosis.

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Abstract

Endometriosis is characterized by the ectopic inflammation, growth, and fibrotic changes in the lesion. Previous study indicates that peritoneal bleeding may accelerate inflammation partially through the activation of protease-activated receptor (PAR) and the prostaglandin (PG) EP2 receptor in endometriosis-like graft of the mouse model. To explore the involvement of hypoxia and/or the inflammatory mediators in epithelial-mesenchymal transition (EMT) of endometrial cells, we examined the effects of thrombin, a PAR agonist and PGE2 on EMT marker expression and cell migration in human endometrial stromal (EtsT499) and epithelial (EM-1) cells. The endometrial cells in 3D culture system incubated for 18 h under hypoxia were cultured in the presence or absence of the combined treatment of thrombin and PGE2 (Throm/PG) for 72 h. Hypoxic conditions increased expression of CXCR4, an EMT marker in EM-1, but not in EtsT499, whereas Throm/PG did not affect CXCR4 in both cells. Throm/PG treatment promoted the migration of EM-1 under hypoxia. Thus, Throm/PG stimulation under hypoxia enhanced CXCR4 expression and accelerated migration of the endometrial epithelial cells. Our data suggests that the inflammatory mediators in retrograde menstrual fluid may be associated with the pathophysiology of ectopic endometrial EMT and migration.
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第93回日本薬理学会年会 セッションID: 93_1-SS-12 会議情報 主催: 第93回日本薬理学会年会 会議名: 第93回日本薬理学会年会 回次: 93 開催地: Yokohama 開催日: 2020/03/16 - 2020/03/18 学生セッション 子宮内膜細胞における低酸素によるEMT関連因子CXCR4発現の上昇 詳細 抄録 Endometriosis is characterized by the ectopic inflammation, growth, and fibrotic changes in the lesion. Previous study indicates that peritoneal bleeding may accelerate inflammation partially through the activation of protease-activated receptor (PAR) and the prostaglandin (PG) EP2 receptor in endometriosis-like graft of the mouse model. To explore the involvement of hypoxia and/or the inflammatory mediators in epithelial-mesenchymal transition (EMT) of endometrial cells, we examined the effects of thrombin, a PAR agonist and PGE2 on EMT marker expression and cell migration in human endometrial stromal (EtsT499) and epithelial (EM-1) cells. The endometrial cells in 3D culture system incubated for 18 h under hypoxia were cultured in the presence or absence of the combined treatment of thrombin and PGE2 (Throm/PG) for 72 h. Hypoxic conditions increased expression of CXCR4, an EMT marker in EM-1, but not in EtsT499, whereas Throm/PG did not affect CXCR4 in both cells. Throm/PG treatment promoted the migration of EM-1 under hypoxia. Thus, Throm/PG stimulation under hypoxia enhanced CXCR4 expression and accelerated migration of the endometrial epithelial cells. Our data suggests that the inflammatory mediators in retrograde menstrual fluid may be associated with the pathophysiology of ectopic endometrial EMT and migration. © 2020 本論文著者

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