Interleukin-1 inhibits growth of normal human endometrial stromal cells

• Published in: Obstetrics and gynecology (New York. 1953) Vol. 80; no. 3 Pt 1; p. 405
• Main Authors: Van Le, L, Oh, S T, Anners, J A, Rinehart, C A, Halme, J
• Format: Journal Article
• Language: English
• Published: United States 01.09.1992
• Subjects: Cell Division - drug effects; Cells, Cultured; DNA - biosynthesis; Endometrium - cytology; Endometrium - drug effects; Female; Humans; Indomethacin - pharmacology; Interleukin-1 - pharmacology; Interleukin-1 - physiology; Thymidine - metabolism; Tritium
• ISSN: 0029-7844

To understand growth regulation of the endometrium by studying the effect of interleukin-1 beta (IL-1) on human endometrial stromal cell proliferation in vitro. Endometrial stromal cells from human endometrium were separated and purified and placed in culture. Fresh and first- and sixth-passage cells were incubated with IL-1 (0.025, 0.25, and 2.5 ng/mL) for 24, 48, and 72 hours, respectively. Proliferation as a function of DNA synthesis was assessed by measuring 3H-thymidine incorporation. Experiments were then repeated in the presence of indomethacin to determine whether IL-1 effects were dependent upon prostaglandin synthesis. We evaluated overall growth by adding IL-1 to cell cultures of sixth-passage stromal cells every 3 days and by performing cell count studies. Interleukin-1 beta significantly inhibited 3H-thymidine uptake in freshly explanted endometrial stromal cells at all doses in a dose-dependent manner; a 44% inhibition was seen at 2.5 ng/mL IL-1 after 72 hours of incubation. In first- and sixth-passage cells, 3H-thymidine uptake was inhibited only at intermediate and high doses of IL-1. Cell count studies showed that sixth-passage cells were significantly inhibited by IL-1 after 23 days of growth (22%; P less than .01). Adding indomethacin did not affect inhibition of growth. Interleukin-1 beta inhibits growth of normal human endometrial stromal cells in vitro and does not appear to be mediated by arachidonic acid metabolites. This inhibition of growth may be important for maintenance of a normal endometrial phenotype.