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The Journal of Clinical Endocrinology & Metabolism Vol. 84, No. 8 2802-2806
Copyright © 1999 by The Endocrine Society


Original Studies

Human Umbilical Vein Endothelial Cells: A New Source and Potential Target for Corticotropin-Releasing Factor

T. Simoncini, R. Apa, F. M. Reis, F. Miceli, M. Stomati, L. Driul, A. Lanzone, A. R. Genazzani and F. Petraglia

Department of Reproductive Medicine and Child Development, Division of Obstetrics and Gynecology, University of Pisa (T.S., M.S., A.R.G.), and Scuola Superiore di Studi e di Perfezionamento S. Anna (T.S.), Pisa; the Institute of Obstetrics and Gynecology, Catholic University (R.A., F.M.), Rome; OASI Institute of Research (A.L.), Troina; and the Department of Surgery, Chair of Obstetrics and Gynecology University of Udine (F.M.R., L.D., F.P.), 33100 Udine, Italy

Address all correspondence and requests for reprints to: Felice Petraglia, M.D., Department of Surgery, Chair of Obstetrics and Gynecology, University of Udine, 33100 Udine, Italy. E-mail: felice.petraglia{at}dsc.uniud.it

Corticotropin-releasing factor (CRF) plays a key role in the modulation of fetal-placental unit function during human pregnancy. CRF has a potent vasoactive action on fetal-placental circulation. As products secreted from endothelial cells affect vascular wall reactivity, we investigated whether cultured human umbilical vein endothelial cells (HUVEC) may represent a source and a target for CRF. With RT-PCR we showed that HUVEC express CRF and CRF receptor type 2 messenger ribonucleic acids. Cultured HUVEC also released CRF peptide in a time-dependent way, and the CRF release was differently regulated by various molecules. Dexamethasone decreased CRF release, whereas progesterone and 17ß-estradiol markedly increased it. Forskolin and PGF2{alpha} were potent stimulators of CRF release from HUVEC. Among the peptides, CRF secretion was stimulated by interleukin-1ß and by endothelin-1.

Our study shows for the first time that HUVEC express CRF messenger ribonucleic acid and peptide as well as the CRF R2 gene, and that CRF release is differentially regulated by several distinct molecules. We here propose that CRF has a role in the regulation of the fetal-placental circulation.




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