Expression of Matrix Metalloproteinase-2 and Tissue Inhibitor of Metalloproteinase-2 Compared with ER and PR Expressions in the Endometriosis and Adenomyosis.
- Author:
Dae Woon EOM
1
;
Gil Hyun KANG
;
Han Moie PARK
;
Sang Su LEE
;
U Seog SON
;
Ok Jun LEE
;
Jung Ran KIM
Author Information
1. Department of Pathology, Ulsan University College of Medicine, Gangneung Asan Hospital, Gangneung, Korea.
- Publication Type:Original Article
- Keywords:
Endometriosis;
Adenomyosis;
Matrix metalloproteinase-2;
Tissue inhibitor of metalloproteinase-2
- MeSH:
Adenomyosis*;
Blotting, Western;
Endometriosis*;
Endometrium;
Epithelial Cells;
Epithelium;
Estrogens;
Female;
Gelatinases;
Matrix Metalloproteinase 2*;
Menstrual Cycle;
Progesterone;
Receptors, Progesterone;
Stromal Cells;
Tissue Inhibitor of Metalloproteinase-2*
- From:Korean Journal of Obstetrics and Gynecology
2004;47(10):1965-1974
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
OBJECTIVE: This study was aimed to investigate the role of matrix metalloproteinase-2 (MMP-2) and inhibitor of metalloproteinase-2 (TIMP-2) for pathogenesis of endometriosis and adeonomyosis by the comparison of their expressions with those of ER (nuclear estrogen receptor) and PR (nuclear progesterone receptor) according to menstrual cycle. METHODS: Twenty seven cases of endometriosis, twenty four cases of adenomyosis,and twenty four cases of normal endometrium were classified by menstrual cycle (proliferative phase, early to mid secretory phase, and late secretory phase to menstrual period) and immunohistochemical study for ER, PR, MMP-2 (72 kD, gelatinase A), and TIMP-2 and Western immunoblotting for MMP-2 and TIMP-2 were performed. RESULTS: The results revealed increased expressions of MMP-2 and TIMP-2 in the epithelial cells of endometriosis throughout cycle compared with uterine endometrium. Expression of MMP-2 and TIMP-2 was weak in adenomyosis. In the epithelium of endometriosis, MMP-2 and ERrevealed a statistical significance each other (p<0.01). Expression of MMP-2 and TIMP-2 in both epithelium and stromal cells of endometriosis of stage 4 was higher than that of stage 1-3 and the expression of MMP-2 in epithelium and stage were statistically significance (p<0.05). PR expression tended to being reduced in both epithelial and stromal cells of endometriosis compared with normal uterine endometrium, except for late secretory phase. Expression of estrogen and progesterone receptors was weak in adenomyosis. By Western immunoblotting study, MMP-2 expression in endometriosis was higher than normal reproductive endometrium. CONCLUSION: The results suggest that the increased expression of MMP-2 associated with the ER expression in epithelium of endometriosis compared with normal endometrium is closely related with the pathogenesis and progression of the endometriosis. Adenomyosis may be associated with different mechanism such as invagination of basal layer of endometrium.
