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Corticotropin-Releasing Hormone Gene Expression in Primary Placental Cells Is Modulated by Cyclic Adenosine 3',5'-Monophosphate¹

Mothers and Babies Research Center, Endocrine Unit, John Hunter Hospital, Newcastle, New South Wales 2310, Australia

Address all correspondence and requests for reprints to: Dr. Roger Smith, Mothers and Babies Research Center, Endocrine Unit, John Hunter Hospital, Newcastle, New South Wales 2310, Australia. E-mail: mdrsm{at}mail.newcastle.edu.au.

CRH, the principal neuropeptide regulator of pituitary ACTH secretion, is also expressed in placenta. Placental CRH has been linked to the process of human parturition. However, the mechanisms regulating transcription of the CRH gene in placenta remain unclear. cAMP signaling pathways play important roles in regulating the expression of a diverse range of endocrine genes in the placenta. Therefore, we have explored the effect of cAMP on CRH promoter activity in primary cultures of human placental cells. Both forskolin and 8-bromo-cAMP, activators of protein kinase A, can increase CRH promoter activity 5-fold in transiently transfected human primary placental cells, in a manner that parallels the increase in endogenous CRH peptide. Maximal stimulation of CRH promoter activity occurs at 500 µmol/L 8-bromo-cAMP and 10 µmol/L forskolin. Electrophoretic mobility shift assay and mutation analysis combined with transient transfection demonstrate that in placental cells cAMP stimulates CRH gene expression through a cAMP regulatory element in the proximal CRH promoter region and involves a placental nuclear protein interacting specifically with the cAMP regulatory element.

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