Results
| PMID | 21613300 |
| Gene Name | PTGS2 |
| Condition | Endometriosis |
| Association |
Associated |
| Population size | 20 |
| Population details | 20 (10 women with endometriosis, 10 control women) |
| Sex | Female |
| Associated genes | COX-2, CDX1, SHP, HIF-1 |
| Other associated phenotypes |
Endometriosis |
|
Mol Hum Reprod. 2011 Nov;17(11):710-9. doi: 10.1093/molehr/gar036. Epub 2011 May Kim, Ki Hyung| Kim, Hye Young| Kim, Hyeong Hoe| Lee, Kyu Sup| Cheong, Jaehun Department of Obstetrics and Gynecology, Pusan National University School of Medicine, Medical Research Institute, Pusan National University Hospital, Busan, Korea. 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)-1alpha 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-1alpha 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. Mesh Terms: Adult| Cell Line| Cyclooxygenase 2/genetics/*metabolism| Endometriosis/enzymology/*physiopathology| Endometrium/enzymology/*metabolism| Female| Gene Expression Regulation| Homeodomain Proteins/*metabolism| Humans| Hypoxia/*physiopathology| Recep |
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