子宮内膜症の生化学的特性に関する基礎ならびに臨床的研究 : 正常子宮内膜との対比 (<シンポジウム> 子宮内膜症をめぐる諸問題)

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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 tyrosin residues of 170 kd protein in the both 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 standarlized 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. Interleukin 1, a kind of cytokine derived from macrophage is detected in over 40% of PF with endometriosis whereas it hardly detected in PF without endometriosis. The levels of t-PA and fibronectin are significantly higher in PF with endometriosis. Furthermore, these two substances at physiological levels have mitogenic potency for endometriotic cells, suggestive of the presence of vicious cycle for progression of endometriosis in its microenvironment. 5. Infertility associated with endometriosis PF with endometriosis includes the substance to inhibit the fertilization of mouse gametes. The substance seems to act on the sperm and decreases its motility and inhibits acrosomal reaction, thus hampering its fertilizability. PF with endometriosis also inhibits the development of the mouse early embryos by interacting with fallopian tubes. Putative substance for this action may be interleukin 1 present in PF with endometriosis. Progesterone levels at midluteal phase are significantly lower in infertile women with endometriosis as compared to those without apparent factors for infertility. Elevated interleukin 1 may be responsible for low levels of progesterone since it is shown to suppress the activity of aromatase and the production of progesterone in cultured granulosa cells. Endometrium with endometriosis is found to have lesser glycogen compared with that without endometriosis. This may be partly related to impaired fecundity associa
社団法人日本産科婦人科学会の論文
1989-08-01

子宮内膜症の生化学的特性に関する基礎ならびに臨床的研究 : 正常子宮内膜との対比 (<シンポジウム> 子宮内膜症をめぐる諸問題)

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