Expression of Inducible Microsomal Prostaglandin E Synthase in Local Lesions of Endometriosis Patients
Article first published online: 7 FEB 2007
American Journal of Reproductive Immunology
Volume 57, Issue 3, pages 218–226, March 2007
How to Cite
Chishima, F., Hayakawa, S., Yamamoto, T., Sugitani, M., Karasaki-Suzuki, M., Sugita, K. and Nemoto, N. (2007), Expression of Inducible Microsomal Prostaglandin E Synthase in Local Lesions of Endometriosis Patients. American Journal of Reproductive Immunology, 57: 218–226. doi: 10.1111/j.1600-0897.2006.00466.x
- Issue published online: 7 FEB 2007
- Article first published online: 7 FEB 2007
- Submitted September 2, 2006; revised November 26, 2006; accepted December 4, 2006.
- microsomal prostaglandin E synthase;
- prostaglandin E2
Recently, an inducible microsomal human prostaglandin E synthase (mPGES) was identified. This enzyme converts the cyclooxygenase (COX) product, prostaglandin (PG) H2, to PGE2, an eicosanoid linked to carcinogenesis. Although elevated levels of PGE2 have been observed in many tumor types including colorectal adenomas and cancers, its role in the pathophysiology of endometriosis is unknown. We previously reported increased expression of COX-2 messenger RNA (mRNA) in local lesions of endometriosis. To further elucidate the mechanism responsible for the elevated levels of PGE2 in endometriosis, we examined the expression levels of mPGES.
Method of study
Samples were obtained from 28 patients, fixed in formalin, and embedded in paraffin for immunohistochemical analysis. We examined the expression of mPGES mRNA in seven cases by reverse transcriptase-polymerase chain reaction using total RNA extracted from frozen samples.
Immunohistochemistry revealed increased mPGES immunoreactivity in endometriosis samples compared with eutopic endometria. Microsomal PGES immunoreactivity was observed in both epithelial cells and stromal or inflammatory cells of endometriosis. Increased expression of mPGES-1 mRNA was detected in most of the endometriosis samples.
Our results suggest that expression of mPGES in addition to COX-2 plays a role in increasing PGE2 production in endometriosis.