Results
| PMID | 11804955 |
| Gene Name | IL1R2 |
| Condition | Endometriosis |
| Association |
Associated |
| Population size | 79 |
| Population details | 79 (26 normal women, 53 various degrees of endometriosis) |
| Sex | Female |
| Associated genes | IL-1RII |
| Other associated phenotypes |
Endometriosis |
|
Biol Reprod. 2002 Feb;66(2):401-6. Kharfi, A| Boucher, A| Akoum, A Unite d'Endocrinologie de la Reproduction, Centre de Recherche, Hopital Saint-Francois d'Assise, Centre Hospitalier Universitaire de Quebec, Universite Laval, Quebec, Quebec, Canada G1L 3L5. Interleukin 1 (IL-1) is a major proinflammatory cytokine that is believed to play a central role in the pathophysiology of endometriosis. The IL-1 receptor type II (IL-1RII) is known to bind to IL-1 and to inhibit its biological effects. In our previous studies, we showed that human endometrium expresses IL-1RII, and we observed reduced expression of the protein in women with endometriosis. The aim of this study was to investigate IL-1RII mRNA in the endometrial tissue of normal women (n = 26) and of patients with various degrees of endometriosis (n = 53). In situ hybridization showed that IL-1RII mRNA expression was significantly decreased in endometriosis, particularly during the early stages of the disease (stages I and II). This was quite obvious in both glandular and stromal cells, and it was corroborated by reverse transcription-polymerase chain reaction analysis of IL-1RII mRNA in the endometrial tissue of women with (n = 10) and without (n = 8) endometriosis. The reduced levels of IL-1RII mRNA in the endometrium of women suffering from endometriosis reveals a profound defect in IL-1RII gene expression and, consequently, a reduced capability of endometrial tissue to down-regulate IL-1 activity. Defective IL-1RII gene expression during the early stages of endometriosis (stages I and II) may contribute to the etiology of the disease. Mesh Terms: Adult| Blotting, Southern| Coloring Agents| Endometriosis/*genetics/pathology| Endometrium/*metabolism/pathology| Female| Glyceraldehyde-3-Phosphate Dehydrogenases/metabolism| Humans| In Situ Hybridization| Interleukin-1/biosynthesis| RNA, Messe |
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