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This version published online on February 9, 2006
Endocrinology, doi:10.1210/en.2005-1626
A more recent version of this article appeared on May 1, 2006
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Submitted on December 20, 2005
Accepted on January 27, 2006

Enhancement of cortisol-induced 11{beta}-hydroxysteroid dehydrogenase type 1 expression by interleukin 1-{beta} in cultured human chorionic trophoblast cells

Wenjiao Li, Lu Gao, Yan Wang, Tao Duan, Leslie Myatt, and Kang Sun*

School of Life Sciences, The First Maternal and Fetal Care Hospital, Fudan University, Second Military Medical University, Shanghai 200433, China; Department of Obstetrics and Gynecology, College of Medicine, University of Cincinnati, Cincinnati, OH 45267, United States

* To whom correspondence should be addressed. E-mail: sunkang2000{at}yahoo.com.

Chorion is the most abundant site of 11{beta}-hydroxysteroid dehydrogenase type 1 (11{beta}-HSD1) expression within intrauterine tissues. It is important to study the regulation of 11{beta}-HSD1 expression in the chorion in terms of local cortisol production during pregnancy. Using real time PCR and enzyme activity assay, we found that cortisol (1 µM) and interleukin 1{beta} (IL-1{beta}) for 24 h significantly increased 11{beta}-HSD1 mRNA expression and reductase activity in cultured human chorionic trophoblasts. A further significant increase of 11{beta}-HSD1 mRNA expression and reductase activity was observed with co-treatment of cortisol and IL-1{beta}. To explore the mechanism of induction, 11{beta}-HSD1 promoter was cloned into pGL3 plasmid expressing a luciferase reporter gene. By transfecting the constructed vector into WISH cells, an amnion-derived cell line, we found that cortisol (1 µM) or IL-1{beta} (10 ng/ml) significantly increased reporter gene expression. Likewise, a further increase in reporter gene expression was observed with co-treatment of cortisol and IL-{beta}. To explore the physiological significance of 11{beta}-HSD1 induction in the chorion, we studied the effect of cortisol on cytosolic phospholipase A2 (cPLA2) and cyclooxygenase 2 (COX-2) expression. We found that treatment of chorionic trophoblast cells with cortisol (1 µM) induced both cPLA2 and COX-2 mRNA expression. We conclude that cortisol up-regulates 11{beta}-HSD1 expression through induction of promoter activity and the effect was enhanced by IL-1{beta}, suggesting that more biologically active glucocorticoids could be generated in the fetal membranes in the presence of infection, which may consequently feed forward in up-regulation of prostaglandin synthesis.
Key words: glucocorticoids • pro-inflammatory cytokines • infection • 11{beta}-hydroxysteroid dehydrogenase type 1 • chorion




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