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Expression of Inducible Microsomal Prostaglandin E Synthase in Local Lesions of Endometriosis Patients
Author(s) -
Chishima Fumihisa,
Hayakawa Satoshi,
Yamamoto Tatsuo,
Sugitani Masahiko,
KarasakiSuzuki Miki,
Sugita Kenji,
Nemoto Norimichi
Publication year - 2007
Publication title -
american journal of reproductive immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.071
H-Index - 97
eISSN - 1600-0897
pISSN - 1046-7408
DOI - 10.1111/j.1600-0897.2006.00466.x
Subject(s) - endometriosis , prostaglandin , atp synthase , microsome , prostaglandin e , chemistry , prostaglandin e2 , endocrinology , medicine , enzyme , biology , andrology , biochemistry
Problem Recently, an inducible microsomal human prostaglandin E synthase (mPGES) was identified. This enzyme converts the cyclooxygenase (COX) product, prostaglandin (PG) H 2 , to PGE 2 , an eicosanoid linked to carcinogenesis. Although elevated levels of PGE 2 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 PGE 2 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. Results 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. Conclusion Our results suggest that expression of mPGES in addition to COX‐2 plays a role in increasing PGE 2 production in endometriosis.