Hypoxia induces expression of COX-2 through the homeodomain transcription factor CDX1 and orphan nuclear receptor SHP in human endometrial cells

Ki Hyung Kim, Hye Young Kim, Hyeong Hoe Kim, Kyu Sup Lee, Jaehun Cheong
Molecular human reproduction · 2011 · vol. 17(11) , pp. 710–719 · doi:10.1093/molehr/gar036 · PMID:21613300 · W2130833461
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Hypoxia in endometrial cells induces COX-2 expression via the transcription factors CDX1 and SHP, which are themselves induced by hypoxia-inducible factor-1α.

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Abstract

Endometriosis, the presence of ectopic endometrial tissue outside the uterine cavity, is a common disease affecting women during their reproductive years. The aim of this study was to identify the molecular mechanism of transcriptional regulation of inflammatory cyclooxygenase-2 (COX-2) gene during endometriosis by hypoxia. Hypoxia induced COX-2 expression in endometrial cells together with the induction of the orphan nuclear receptor SHP and intestinal-specific transcription factor Caudal-related transcription factor 1 (CDX1). Hypoxia-inducible factor (HIF)-1α was responsible for SHP induction mediated by a hypoxia. In addition, we observed that ectopic expression of CDX1 enhanced COX-2 gene expression in hypoxia-dependent fashion. Additionally, we evaluated that induction of CDX1 by hypoxia was mediated by SHP. Expression of COX-2, CDX1, SHP and HIF-1α mRNA in hypoxia-treated human endometrial cells were significantly higher than normal control cells. These results suggest that the SHP and CDX1 expression increased by hypoxia play an active role in inducing inflammatory COX-2 expression in the pathogenesis of endometriosis.

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Condition tags

endometriosis

MeSH descriptors

Cyclooxygenase 2 Endometriosis Endometrium Homeodomain Proteins Hypoxia Receptors, Cytoplasmic and Nuclear Adult Cell Line Cyclooxygenase 2 Cyclooxygenase 2 Endometriosis Endometriosis Endometrium Endometrium Female Gene Expression Regulation Homeodomain Proteins Humans Hypoxia Receptors, Cytoplasmic and Nuclear

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organisms 2
human human

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