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Published on: May 23, 2014
Interleukin-1 inhibits growth of normal human endometrial stromal cells
1Department of Obstetrics and Gynecology, University of North Carolina, Chapel Hill.
Insights
Interleukin-1 beta inhibits human endometrial stromal cell proliferation in vitro. This growth regulation is not dependent on prostaglandin synthesis and may be crucial for maintaining a normal endometrial phenotype.
Area of Science:
- Reproductive biology
- Cell biology
- Immunology
Background:
- Endometrial growth regulation is complex.
- Interleukin-1 beta (IL-1) is a cytokine with potential roles in endometrial function.
Purpose of the Study:
- To investigate the effect of IL-1 on human endometrial stromal cell proliferation in vitro.
- To determine if IL-1 mediated effects on endometrial cells depend on prostaglandin synthesis.
Main Methods:
- Human endometrial stromal cells were cultured and treated with varying doses of IL-1.
- Proliferation was assessed via 3H-thymidine incorporation and cell counts.
- Experiments were repeated with indomethacin to assess prostaglandin involvement.
Main Results:
- IL-1 significantly inhibited DNA synthesis in freshly isolated cells in a dose-dependent manner.
- Proliferation of passaged cells was inhibited by IL-1, particularly at higher doses.
- IL-1 inhibited overall cell growth over 23 days, independent of prostaglandin synthesis.
Conclusions:
- IL-1 inhibits the growth of human endometrial stromal cells in vitro.
- This inhibitory effect is not mediated by arachidonic acid metabolites.
- IL-1's growth-inhibitory action may be vital for maintaining the normal endometrial phenotype.
Objective:
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.
Methods:
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.
Results:
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.
Conclusion:
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.
