| Co-Investigator(Kenkyū-buntansha) |
MARUYAMA Tetsuo Keio University, School of Medicine, Assistant Professor, 医学部, 講師 (10209702)
KOSAKI Kenjiro Keio University, School of Medicine, Associte Professor, 医学部, 助教授 (30234743)
YOSHIMURA Yasunori Keio University, School of Medicine, Professor, 医学部, 教授 (10129736)
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| Research Abstract |
Endometriosis is a common disease defined as the growth of endometrial tissue outside the uterine cavity that often results in gynecological problems including chronic pelvic pain, dysmenorrhoea and infertility. However, despite extensive studies, the etiology and pathophysiology are not fully understood.
To examine the estrogen(E) and progesterone(P) withdrawal for the development of endometriosis, we investigated genes that were differentially expressed among endometrium without E and P(CO), endometrium with E and P(EP), and steroid withdrawn endometrium(WD) using complementary DNA microarrey. A total of 13 genes were indentified as up-regulated and 32 genes were identified as down-regulated in WD compared with CO and EP. MCP-1,IL-8,EST-X(not identified), and MMP-8 were up-regulated in WD. Changes in three genes, IL-8,MCP1 and EST-X, which were up-regulated in WD, were verified using RT-PCR. We investigated the expression of MMP-8, and EST-X in eutopic endometrium and ectopic endometrial tissue. We also investigated gene expression of Lox-5,cPGES, and Kinin B1R which were reported to play an important role in inflammation and hyperalgesia. Both eutopic and ectopic endometrial tissue expressed MMP-8,EST-X, and Lox-5. Ectopic endometrial tissue had higher EST-X,MMP-8, and Lox-5 expression.
These results provide new insighs into the role of steroids withdrawal for the pathophysiology of endometriosis. Steroids withdrawal model may be an invaluable tool for identifying the endometriosis related genes. The genes which regulate the development of ectopic endometrium require further investigation, EST-X,MMP-8, and Lox-5 are good candidate for the investigation of pathophysiology of endometriosis.
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