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Matrix metalloproteinase-2, membranous type 1 matrix metalloproteinase, and tissue inhibitor of metalloproteinase-2 expression in ectopic and eutopic endometrium

Title
Matrix metalloproteinase-2, membranous type 1 matrix metalloproteinase, and tissue inhibitor of metalloproteinase-2 expression in ectopic and eutopic endometrium
Authors
Chung H.W.Lee J.Y.Moon H.-S.Hur S.E.Park M.H.Wen Y.Polan M.L.
Ewha Authors
정혜원문혜성
SCOPUS Author ID
정혜원scopus; 문혜성scopus
Issue Date
2002
Journal Title
Fertility and Sterility
ISSN
0015-0282JCR Link
Citation
Fertility and Sterility vol. 78, no. 4, pp. 787 - 795
Indexed
SCI; SCIE; SCOPUS WOS scopus
Document Type
Conference Paper
Abstract
Objective: To investigate expression of matrix metalloproteinase-2 (MMP-2), membranous type 1 matrix metalloproteinase (MT1-MMP), and tissue inhibitor of metalloproteinase-2 (TIMP-2) in ectopic and eutopic endometrium from women with and without endometriosis throughout the menstrual cycle. Design: Molecular studies in human tissue. Setting: Reproductive immunology laboratory of a university medical center. Patient(s): Fifty-three premenopausal woman (23 with endometriosis and 30 without endometriosis) undergoing laparoscopic surgery. Endometrium and ectopic endometriosis tissue were obtained at the time of surgery. Main Outcome Measure(s): Messenger RNA and protein expression from eutopic and ectopic endometrium was analyzed by using quantitative competitive polymerase chain reaction, zymography, and Western blot assay. Result(s): Uterine endometrium from women with endometriosis expressed higher levels of MMP-2 and MT1-MMP and lower levels of TIMP-2 than did endometrium from normal women. Conclusion(s): Eutopic endometrium from patients with endometriosis may be more invasive and prone to peritoneal implantation because of greater expression of MMP-2 and MT1-MMP and lower expression of TIMP-2 messenger RNA, compared with endometrium from women without endometriosis. Thus, increased proteolytic activity may help to explain the invasive factors that result in endometriosis. © 2002 by American Society for Reproductive Medicine.
DOI
10.1016/S0015-0282(02)03322-8
Appears in Collections:
의과대학 > 의학과 > Journal papers
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