[Fundamental and clinical studies on biochemical properties of endometriosis in comparison with endometrium].
1. Regulatory mechanism of cell growth of endometriosis in comparison with endometrium. Estradiol alone has no growth-promoting effect on both endometriotic and endometrial cells. Epidermal growth factor (EGF) stimulates cell growth of both cell types. Endometrial cells but not endometriotic cells produce and release EGF into culture media so that stimulatory effect of exogenous addition of EGF is blunted in endometrial cells. Estradiol exerts its mitogenic action by enhancing the mitogenic effect of EGF in endometrium. By contrast, the effect of estradiol is minimal in endometriotic cells, showing less dependency on estradiol for their proliferation. Progesterone inhibits cell growth of the both cell types in the same manner. 2. A biological role of EGF in endometriosis. Endometriotic cells possess EGF receptors. The affinity of the receptor is the same as that of endometrial cells. However, the number of receptor per cell is about half of that for endometrium. Estradiol increases the number of EGF receptors in endometrial cells which may explain the mitogenic effect of estradiol in the face of EGF. However, stimulatory effect of estradiol for EGF receptors is less pronounced in endometriotic cells. Mitogenic action of EGF is suggested to be mediated by phosphorylation of tyrosine residues of 170 kd protein in the tissues. EGF increases the production of tissue plasminogen activator (t-PA) and activates the aromatase activity of the both cell types. However, the stimulatory action of EGF on progestin receptor is observed only in endometrial cells. 3. Biochemical characterization of endometriotic cells in comparison with endometrial cells. Endometriotic tissues accumulate less amount of glycogen and XIII factor of blood coagulation as compared to endometrial tissues. The ability of endometriotic cells to release prostaglandin is also weaker, suggesting suppressed differentiated function of endometriotic cell. Endometriotic cells produce the same amount of CA125 as endometrial cells. Danazol and EGF inhibit the release of CA125 into culture media when standardized per cell. Therefore, normalization of CA125 levels during the treatment dose not always mean the reduction of the lesions but reflect the suppressed function of the endometriotic tissues. 4. Altered microenvironment of endometriotic tissues. An analysis of peritoneal fluid. The amount of peritoneal fluid (PF) with endometriosis increased throughout the menstrual cycle. A number of macrophage is reported to increase in PF with endometriosis.(ABSTRACT TRUNCATED AT 400 WORDS)
Taketani
Y
Y
Department of Obstetrics and Gynecology, Faculty of Medicine, University of Tokyo.
D000818:Animals; D015295:Antigens, Tumor-Associated, Carbohydrate / Q000032:analysis; D001202:Ascitic Fluid / Q000032:analysis / Q000378:metabolism; D002455:Cell Division / Q000187:drug effects; D004715:Endometriosis / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D004717:Endometrium / Q000166:cytology / Q000276:immunology / Q000378:metabolism*; D004815:Epidermal Growth Factor / Q000096:biosynthesis / Q000494:pharmacology / Q000502:physiology; D066246:ErbB Receptors / Q000378:metabolism; D004958:Estradiol / Q000494:pharmacology; D005169:Factor VIII / Q000378:metabolism; D005260:Female; D006003:Glycogen / Q000378:metabolism; D006801:Humans; D007247:Infertility, Female / Q000209:etiology / Q000378:metabolism; D007375:Interleukin-1 / Q000378:metabolism; D008183:Luteal Phase; D051379:Mice; D011374:Progesterone / Q000378:metabolism / Q000494:pharmacology
D015295:Antigens, Tumor-Associated, Carbohydrate; D007375:Interleukin-1; D011374:Progesterone; D004958:Estradiol; D004815:Epidermal Growth Factor; D005169:Factor VIII; D006003:Glycogen; D066246:ErbB Receptors