The differential expression of intercellular adhesion molecule-1 (ICAM-1) and regulation by interferon-gamma during the pathogenesis of endometriosis

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Abstract

Problem: To establish an in vitro culture model of the endometrium and endometriotic lesions, and demonstrate the different expressions of intercellular adhesion molecule-1 (ICAM-1) in these lesions. Methods: Eight women with moderate to severe stages of endometriosis were enrolled. The specimens were collected from their eutopic endometrium, visually normal peritoneum, ovarian endometrioma and peritoneal endometriotic spots during the follicular phase of the menstrual cycle. ICAM-1 mRNA and protein were expressed by using reverse transcription-polymerase chain reaction, enzyme-linked immunosorbent assay, immunoblot, and immunocytochemistry. Results: The results demonstrate that visually normal peritoneal cells and ovarian endometriomas of endometriotic patients can express high ICAM-1 mRNA. Normal peritoneal cells further expressed significant soluble ICAM-1 protein levels without cytokine stimulation. The eutopic endometrium expressed less soluble ICAM-1 protein, and ICAM-1 expressions increased in cultured stromal cells of eutopic endometrium, ovarian endometrioma, and peritoneal endometriotic spots under interferon-gamma (INF-γ) stimulation. Conclusion: The ICAM-1 expression in visually normal peritoneal cells from women with endometriosis may play a role in the early implantation of peritoneal endometriosis. Peritoneal INF-γ stimulation is significantly associated with ICAM-1 expression in endometriosis. Therefore, the differential expression and changes of ICAM-1 may be involved in the mechanism that can escape immunosurveillance and allow refluxed endometrial cells to spread and invade other location. © Blackwell Munksgaard, 2004.

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Wu, M. H., Yang, B. C., Lee, Y. C., Wu, P. L., & Hsu, C. C. (2004). The differential expression of intercellular adhesion molecule-1 (ICAM-1) and regulation by interferon-gamma during the pathogenesis of endometriosis. American Journal of Reproductive Immunology, 51(5), 373–380. https://doi.org/10.1111/j.1600-0897.2004.00171.x

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