Increased Expression of Cyclooxygenase-2 in Local Lesions of Endometriosis Patients
Article first published online: 19 JUN 2002
American Journal of Reproductive Immunology
Volume 48, Issue 1, pages 50–56, July 2002
How to Cite
CHISHIMA, F., HAYAKAWA, S., SUGITA, K., KINUKAWA, N., ALEEMUZZAMAN, S., NEMOTO, N., YAMAMOTO, T. and HONDA, M. (2002), Increased Expression of Cyclooxygenase-2 in Local Lesions of Endometriosis Patients. American Journal of Reproductive Immunology, 48: 50–56. doi: 10.1034/j.1600-0897.2002.01101.x
- Issue published online: 19 JUN 2002
- Article first published online: 19 JUN 2002
- Submitted September 8, 2001, accepted September 21, 2001
- competitive PCR;
PROBLEM: Human endometrial glands contain the highest levels of cyclooxygenase (COX), although whether it is COX-1 and/or COX-2 has not been previously determined. Overexpression of COX-2 may result in the pathogenesis of endometriosis.
METHOD OF STUDY: Tissue sections were obtained from 28 premenopausal women undergoing laparotomy or laparoscopic surgery for benign conditions. Endometrium, ectopic endometriosis tissue and peritoneum were obtained at the time of surgery. Informed consents were obtained from all the patients participating in this study. Immunohistochemistry was performed on consecutive sections of paraffin-embedded tissue using anti-COX-2 antibody. Expressions of COX-2 mRNA in endometrium, ectopic endometriosis tissue, and peritoneum were quanti-tavely determined by competitive reverse transcription–polymerase chain reaction (RT–PCR).
RESULTS: In the uterus, COX-2 was localized in the endometrial epithelium. Eutopic endometrial surface epithelium contains more COX-2 than does glandular epithelium. We observed more frequent and denser COX-2 staining in the ectopic endometriosis implants when compared with eutopic endometrium. Level of COX-2 mRNA in endometriosis was increased up to five times that of eutopic endometria.
CONCLUSION: Hyper activation of COX-2 with abnormal prostaglandin generation is considered to contribute to the pathophysiology of endometriosis and disease progression.