Menstrual cycle-specific inhibition of endometrial stromal cell proliferation by oncostatin M

• Published in: Molecular human reproduction 2001-07, Vol.7 (7), p.665-670
• Main Authors: Ohata, Yorie, Harada, Tasuku, Fujii, Akiko, Yoshida, Souichi, Iwabe, Tomio, Terakawa, Naoki
• Format: Article
• Language: English
• Subjects: Antigens, CD - genetics; Antigens, CD - metabolism; Biological and medical sciences; Cell Differentiation - drug effects; Cell Division - drug effects; cell proliferation; Cells, Cultured; Cytokine Receptor gp130; differentiation; endometriosis; endometrium; Endometrium - cytology; Endometrium - metabolism; Female; Fundamental and applied biological sciences. Psychology; Hormone metabolism and regulation; Humans; Leukemia Inhibitory Factor Receptor alpha Subunit; Mammalian female genital system; Membrane Glycoproteins - genetics; Membrane Glycoproteins - metabolism; Menstrual Cycle - physiology; Oncostatin M; Peptides - genetics; Peptides - metabolism; Peptides - pharmacology; Receptors, Cytokine - genetics; Receptors, Cytokine - metabolism; Receptors, Oncostatin M; Receptors, OSM-LIF; Stromal Cells - cytology; Stromal Cells - metabolism; Vertebrates: reproduction
• ISSN: 1360-9947; 1460-2407
• DOI: 10.1093/molehr/7.7.665

We have investigated the possible roles of oncostatin M (OSM), which is a member of the interleukin-6 family of cytokines, in endometrial and endometriotic stromal cell growth. Endometrial and endometriotic stromal cells were collected from the uterus or ovarian chocolate cysts. We observed the expression of mRNA transcripts for OSM, OSM receptor subunit β, leukaemia inhibitory factor receptor subunit (LIFR), and glycoprotein 130 in endometrial and endometriotic stromal cells. We also examined the effects of OSM (0–50 ng/ml) and LIF (0–10 ng/ml) on endometrial and endometriotic stromal cell proliferation and evaluated the effects of OSM on endometrial stromal cell differentiation. The presence of 10–50 ng/ml OSM significantly suppressed endometrial stromal cell growth in secretory phase tissue but not in proliferative phase tissue. In contrast, stromal cells in endometriotic tissues were resistant to the inhibitory effects of OSM. Addition of LIF did not influence the growth of endometrial stromal cells. We also showed that 10 ng/ml OSM stimulated markers of differentiation causing increased prolactin secretion and cyclooxygenase-2 gene expression in endometrial stromal cells from the secretory phase. These results suggest that OSM may play a pivotal role in regulating the growth and differentiation of endometrial cells. Endometriotic cells may behave differently from normal endometrial cells in terms of the inhibitory response to OSM.