Secretion of monocyte chemotactic protein-1 by cytokine-stimulated endometrial cells of women with endometriosis. Le groupe d'investigation en gynécologie
- PMID: 7843438
- DOI: 10.1016/s0015-0282(16)57363-4
Secretion of monocyte chemotactic protein-1 by cytokine-stimulated endometrial cells of women with endometriosis. Le groupe d'investigation en gynécologie
Abstract
Objective: To evaluate in vitro the production of monocyte chemotactic protein-1 (MCP-1) by endometrial cells of patients with and without endometriosis.
Design: Primary cultures of stromal and epithelial cells isolated from human endometrium were exposed during 24 hours to different cytokines. Monocyte chemotactic protein-1 secretion was analyzed in the culture medium.
Setting: Gynecology clinic and laboratories of endocrinology of reproduction and immunology.
Patients: Women presenting for infertility or pelvic pain in which endometriosis was diagnosed at laparoscopy (n = 6) and women presenting for tubal ligation without laparoscopic evidence of the disease (n = 6).
Interventions: None.
Main outcome measures: De novo secretion of MCP-1 in the culture supernatant by immunoprecipitation and sodium dodecyl sulfate-polyacrylamide gel electrophoresis after metabolic labeling with 35S-cysteine.
Results: The incubation of endometrial epithelial cells of endometriosis women with either interleukin-1 beta or tumor necrosis factor-alpha resulted in the appearance of at least two and sometimes three bands having approximately 15, 13, and 9 kd molecular weights. These bands were identified as three distinct species of MCP-1 as their immunoprecipitation was prevented effectively in presence of an excess of cold MCP-1. In contrast, the endometrial epithelial cells of only one of six normal women produce significant levels of MCP-1 under the same stimulation conditions. The stromal cells of both groups of subjects do not secrete appreciable amounts of MCP-1 or only small quantities in two cases of endometriosis.
Conclusions: Monocyte chemotactic protein-1 secretion is upregulated in cytokine-stimulated endometrial epithelial cells of women having endometriosis as compared with normal women without evidence of the disease. Such a difference at the level of eutopic endometrial cell may have a significance in the physiopathology of endometriosis.
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