Distinct expression of the soluble and the membrane-bound forms of interleukin-1 receptor accessory protein in the endometrium of women with endometriosis  

Oleh:

Guay, Sophie ; Michaud, Nadège ; Bourcier, Nathalie ; Leboeuf, Mathieu ; Lemyre, Madeleine ; Mailloux, Jacques

Jenis: Article from Journal - ilmiah internasional
Dalam koleksi: Fertility and Sterility (keterangan: ada di ClinicalKey) vol. 95 no. 04 (Mar. 2011), page 1284-1290.
Topik: ENDOMETRIUM; Endometriosis; endometrium; IL-1; IL1RAcP

Ketersediaan

Perpustakaan FK Nomor Panggil: F02.K.2011.03 Non-tandon: 1 (dapat dipinjam: 0) Tandon: tidak ada

Lihat Detail Induk

Isi artikel

Objective To investigate interleukin (IL) 1 receptor accessory protein (IL1RAcP) expression in the eutopic endometrium of women with endometriosis. Design Retrospective study. Setting Human reproduction research laboratory. Patient(s) Sixty-six women with endometriosis and 60 healthy women with no laparoscopic evidence of endometriosis. Intervention(s) Endometrial tissue samples were obtained during laparoscopic surgery. Main Outcome Measure(s) IL1RAcP protein expression was analyzed by immunohistochemistry, Western blot, and ELISA, and IL1RAcP mRNA expression was analyzed by quantitative real-time polymerase chain reaction. Result(s) This study showed a significant downregulation of soluble (s)IL1RAcP expression in the eutopic endometrium of women with endometriosis compared to normal women, occurring at the protein or mRNA level. This finding appeared to vary according to endometriosis stage, being more obvious in the earliest (I and II) than the latest (III and IV) stages of the disease. However, the membrane-bound IL1RAcP did not show any noticeable endometriosis-related change, neither at the protein or mRNA level. Conclusion(s) In view of the wide spectrum of IL-1 inflammatory and growth-promoting effects, downregulation of sIL1RAcP, which is known for inhibiting IL1, indicates a profound defect in the capability of endometrial cells of women with endometriosis to counterregulate IL-1 effects and may represent an important mechanism underlying the ability of these cells to implant and develop into host tissues.

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