Results
| PMID | 17454161 |
| Gene Name | STS |
| Condition | Endometriosis |
| Association |
Associated |
| Population size | 25 |
| Population details | 25 (16 samples of ovarian endometriosis, 9 of normal endometrium) |
| Sex | Female |
| Associated genes | Aromatase, 17beta-HSD types 1, 17beta-HSD types 7, sulfatase, Erbeta, Eralpha |
| Other associated phenotypes |
Endometriosis |
|
Gynecol Endocrinol. 2007 Feb;23(2):105-11. Smuc, Tina| Pucelj, Martina Ribic| Sinkovec, Jasna| Husen, Bettina| Thole, Hubert| Lanisnik Rizner, Tea Institute of Biochemistry, Faculty of Medicine, University of Ljubljana, Vrasov trg. 2, 1000 Ljubljana, Slovenia. Endometriosis is defined as the presence of endometrial glands and stroma within extrauterine sites, and it is well known that endometriosis is an estrogen-dependent disease. The defective formation and metabolism of steroid hormones is responsible for the promotion and development of endometriosis. In the present study we examined the mRNA levels of six enzymes that are involved in the metabolism of estrogen and progesterone--aromatase, 17beta-hydroxysteroid dehydrogenase (17beta-HSD) types 1, 2 and 7, sulfatase and sulfotransferase--and of the steroid receptors--estrogen receptors alpha and beta (ERalpha, ERbeta) and progesterone receptors A and B (PRAB)--implicated in human ovarian endometriosis. We analyzed 16 samples of ovarian endometriosis and 9 of normal endometrium. The real-time polymerase chain reaction analyses revealed that six of the nine genes investigated are differentially regulated. Aromatase, 17beta-HSD types 1 and 7, sulfatase and ERbeta were statistically significantly upregulated, while ERalpha was significantly downregulated, in the endometriosis group compared with the control group. There were no significant differences in 17beta-HSD type 2, sulfotransferase and PRAB gene expression. Our results indicate that, in addition to the previously reported upregulation of aromatase, upregulation of 17beta-HSD types 1 and 7 and sulfatase can also increase the local estradiol concentration. This could thus be responsible for the estrogen-dependent growth of endometriotic tissue. Surprisingly ERalpha was downregulated. Mesh Terms: 17-Hydroxysteroid Dehydrogenases/genetics/*metabolism| Adult| Aromatase/genetics/metabolism| Down-Regulation/genetics| Endometriosis/enzymology/genetics/*metabolism| Estradiol/blood| Estrogen Receptor alpha/genetics/*metabolism| Female| *Gene Expr |
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