Abstract
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 that has been linked to carcinogenesis. Increased amounts of PGE2 have been observed in many tumor types including colorectal adenomas and cancers. We have already reported increased expression of COX‐2 mRNA in local lesions of endometriosis. To further elucidate the mechanism responsible for increased levels of PGE2 in endometriosis, we investigated the expression of mPGES. Formalin fixed and paraffin embedded 15 samples were examined with immunohistochemistry. Immunostaining was carried out with a rabbit mPGES‐1 anti‐human polyclonal antiboby. In selected cases, expression of mPGES mRNA was examined by RT‐PCR using total RNA extracted from frozen samples. Immunohistochemistry revealed increased mPGES immunoreactivity in endometriosis samples compared with eutopic endometria. Immunoreactivity of mPGES was observed in both epithelia and stromal or inflammatory cells. Increased expression of mPGES‐1 mRNA was detected in most of endometriosis samples. Taken together, our results suggested that overexpression of mPGES in addition to COX‐2 contributes to possible increased PGE2 production in endometriosis patients.
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