Endocrinological and immunological study on regulatory mechanism of human endometrial differentiation

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Human endometrium was obtained from the patients with normal menstrual cycles who underwent hysterectomy for the treatment of gynecological diseases. The tissue samples were minsed and incubated in RPMI medium containing 10 % fetal bovine serum, collagenase and DNase. Glandular cells were separated from stromal cells by differential sedimentation. The stromal cells cultured with progesterone decidualized morphologically and secreted prolactin into the culture supernatant. Using this system, the effects of interleukin 1 (IL-1), Macrophage colony-stimulating factor (M-CSF), leukemia inhibitory factor (LIF) and testosterone on the endometrial differentiation were studied. Furthermore, endometrium was examined immunohistologically with monoclonal antibodies against peptidase antigens. The results were as follows:1. IL-1 inhibited morphological decidualization of endometrial stromal cells in vitro, and also reduced prolactin secretion by the cultured endometrial stromal cells in a dose-dependent manner.2. Cultured endometrial stromal cells secreted M-CSF in the presence of progesterone. The expression of M-CSF mRNA was enhanced by the addition of progesterone. Endometrial glandular cells also secreted M-CSF, but it was not under the sex steroidal control.3. LIF was mainly detected on the endometrial glandualr cells.4. Testosterone induced prolactin secretion by the cultured endometrial stromal cells in a dose dependent manner. This prolactin secretion was enhanced by the addition of progesterone.5. Endometrial stromal cells expressed aminopeptidase N and neutral endopeptidase, whereas endometrial glandular cells expressed dipeptidyl peptidase IV. The expression of these peptidase antigens changed during menstrual cycle and pregnancy.