Results
| PMID | 20971605 |
| Gene Name | HOXA10 |
| Condition | Endometriosis |
| Association |
Associated |
| Population size | 32 |
| Population details | 32 (17 infertile women with minimal endometriosis, 15 healthy fertile women) |
| Sex | Female |
| Infertility type | Female infertility |
| Associated genes | HOXA10 |
| Other associated phenotypes |
Female infertility, Endometriosis |
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Biomed Pharmacother. 2010 Dec;64(10):697-705. doi: 10.1016/j.biopha.2010.09.012. Szczepanska, Malgorzata| Wirstlein, Przemyslaw| Luczak, Michal| Jagodzinski, Pawel P| Skrzypczak, Jana Department of Obstetrics, Gynecology and Gynecological Oncology, Division of Reproduction, University of Medical Sciences, 60-781 Poznan, Poland. Recent human and animal studies have suggested that reduced HOXA10 expression in the implantation window of eutopic endometrium may contribute to infertility in women with endometriosis. Therefore, we examined the HOXA10 transcript, protein and HOXA10 promoter methylation levels in midluteal eutopic endometrium from 17 infertile women with minimal endometriosis and 15 healthy fertile women from a Polish cohort. Real-time quantitative PCR (RQ-PCR) and western blotting analysis revealed significantly lower levels of HOXA10 transcript (P=0.019) and protein (P=0.048) levels in eutopic endometrium from infertile women with endometriosis as compared to healthy fertile women. Moreover, sodium bisulfite sequencing of three HOXA10 CpG islands showed significantly higher methylation levels of genomic DNA from midluteal eutopic endometrium from infertile women with endometriosis as compared to healthy fertile women (P=0.006). We confirmed that DNA hypermethylation can be one of the potential molecular mechanisms silencing HOXA10 expression in the midluteal endometrium associated with infertility in women with endometriosis. Mesh Terms: Adult| DNA Methylation| Endometriosis/complications/*genetics/metabolism| Endometrium/metabolism| Female| Gene Silencing| Homeodomain Proteins/biosynthesis/*genetics| Humans| Infertility, Female/etiology/*genetics/metabolism| Promoter Regions, Ge |
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