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Original Studies |
Division of Endocrinology, Childrens Hospital Medical Center and Perinatal Research Institute, University of Cincinnati College of Medicine, Cincinnati, Ohio 45229
Address all correspondence and requests for reprints to: Dr. Stuart Handwerger, Division of Endocrinology, Childrens Hospital Medical Center, 3333 Burnet Avenue, Cincinnati, Ohio 45229-3039. E-mail: stuart.handwerger{at}chmcc.org
PRL is synthesized and released by several extrapituitary tissues, including decidualized endometrial stromal cells. As interleukin-2 (IL-2) stimulates the synthesis and release of pituitary PRL, and decidual stromal cells have receptors for IL-2, we examined whether IL-2 also regulates the release of decidual PRL. Exposure of primary cultures of human decidual cells (106 cells/well) from term pregnancies to IL-2 (50 ng/mL) inhibited PRL release beginning 48 h after exposure. The inhibition by IL-2 was dose dependent, and the maximal inhibition of PRL release after 5 days of exposure to IL-2 was 71.0 ± 0.9% (mean ± SE). IL-2, however, had no effect on decidual cell viability. The inhibitory effect of IL-2 on PRL release was secondary to inhibition of PRL synthesis. Decidualized human endometrial stromal cells transfected with 3 kb of the extrapituitary PRL (exon 1a) promoter coupled to a luciferase expression vector responded to IL-2 (10 ng/mL) with a significant decrease in luciferase activity. These findings strongly suggest that IL-2 inhibits the synthesis and release of decidual PRL and provide further support for a critical role of cytokines in the regulation of decidual PRL gene expression.
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