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Glucocorticoid signaling regulates cell invasion and migration in the human first‐trimester trophoblast cell line Sw.71
Author(s) -
Kisanga Edwina P.,
Tang Zhonghua,
Guller Seth,
Whirledge Shan
Publication year - 2018
Publication title -
american journal of reproductive immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.071
H-Index - 97
eISSN - 1600-0897
pISSN - 1046-7408
DOI - 10.1111/aji.12974
Subject(s) - glucocorticoid , trophoblast , glucocorticoid receptor , biology , placentation , endocrinology , medicine , signal transduction , microbiology and biotechnology , placenta , fetus , genetics , pregnancy
Problem The development of the placenta and its functions are sensitive to infection and stress, which can activate the hypothalamic‐pituitary‐adrenal axis. Adrenally produced glucocorticoids are the body's primary mediators of the inflammatory and stress response. Although the glucocorticoid receptor (GR) is expressed in all human villous trophoblast tissue, the effect of glucocorticoids on placentation is not well understood. Method of study Using microarray analysis, we identified the glucocorticoid‐regulated transcriptional profile in the immortalized first‐trimester extravillous trophoblast cell line Swan.71 (Sw.71). Results The synthetic glucocorticoid dexamethasone significantly regulated 3829 genes, including genes associated with cell movement, growth, and survival. SERPINE1 , an inhibitor of trophoblast invasion, was induced by glucocorticoids in Sw.71 cells and is associated with the pathogenesis of preeclampsia. Glucocorticoid treatment induced recruitment of activated polymerase II and GR to the SERPINE1 promoter, suggesting a mechanism for transcriptional regulation. Functionally, glucocorticoid treatment inhibited cell proliferation, migration, and invasion. Conclusion These findings suggest that glucocorticoids regulate extravillous trophoblast functions by altering the gene expression profile, which may contribute to the pathogenesis of reproductive disorders such as preeclampsia and IUGR.