RE-1 : The expression of Mullerian Inhibiting Substance Type II Receptor (MISRII) in Endometrial hyperplasia = RE-1 : The expression of Mullerian Inhibiting Substance Type II Receptor (MISRII) in Endometrial hyperplasia

국문 초록 (Abstract)

목적: Mullerian inhibiting substance (MIS) is produced in Sertoli cells of fetal testis and causes regression of Mullerian ducts. MIS is well known to act as a regulator of female reproductive function but also inhibits the growth of Mullerian duct-derived tumors in vivo and in vitro. Therefore, this study is aimed to analyze expression of MIS type II receptor (MISRII) and receptor mRNA in normal endometrium compared with endometrial hyperplaslaia, to make foundation of MIS as a biological modifier for treatment endometrial hyperplasia. 방법: The study included 18 human endometrial tissues (10 normal endometrium, 5 simple endometrial hyperplasia without atypia and 3 complex endometrial hyperplasia without atypia). The normal endometrium was classified as proliferative and secretory endometrium according to histologic finding. By Immunohistochemistry, we observed the expression and variation of MISRII protein. And the expression was graded by 2 experienced pathologists and categorized as negative, weakly positive, moderately positive and strongly positive. Reverse transcriptase polymerase chain reaction (RT-PCR) was used to quantify MISRII mRNA expression. 결과: 1. The expression of MISRII protein was observed on all normal endometrium and endometrial hyperplasia tissues. The endometrial hyperplasia showed moderate and strong expression, while normal endometrium showed weak and moderate expression. Among normal endometrium, the potency of MISRII expression was similar. 2. The expression of　MISRII mRNA on normal endometrium and endometrial hyperplasia was evaluated and quantified by RT-PCR. 3. The amount of MISRII mRNA on simple endometrial hyperplasia tissue was 1.40 times more than that of normal endometrium and 1.77 times more on complex endometrial hyperplasia. 결론: This study demonstrates that MISRII is present on normal endometrium and endometrial hyperplasia tissues. The expression of MISRII was similar among normal endometrium but the level of MISRII mRNA was elevated on endometrial hyperplasia. These data suggest that MIS may be used as a biological modifier or therapeutic modulator on endometrial hyperplasia in the future.