Glucocorticoids are implicated in successful blastocyst implantation, whereas alterations in glucocorticoid levels are associated with various pregnancy disorders including preeclampsia. Tissue concentration of active glucocorticoids depends on the expression of 11β-hydroxysteroid dehydrogenase (11β-HSD). This study investigated the contribution of first trimester decidua to glucocorticoid availability at the fetal-maternal interface by assessing the expression and regulation of 11β-HSD in human first trimester decidual tissues and cells and by evaluating 11β-HSD levels in preeclamptic vs. gestational age-matched decidua. 11β-HSD1 was the predominant isoform in first trimester decidua. In vitro, decidual cell 11β-HSD1 levels and enzymatic activity were up-regulated by ovarian steroids and inflammatory cytokines. Higher levels of 11β-HSD1 were found in preeclamptic decidua compared to controls. The present study indicates the predominance of 11β-HSD oxoreductase isoform in early decidua. Observations that ovarian hormones and inflammatory cytokines up-regulate 11β-HSD1, together with increased 11β-HSD1 expression in preeclampsia, highlight a role for decidual cells in controlling biologically active glucocorticoids in early pregnancy.
Keywords: 11beta-HSD; Cytokines; Decidua; Preeclampsia; Steroids.
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