Please use this identifier to cite or link to this item:
|Scopus||Web of Science®||Altmetric|
|Title:||Urocortin: A mechanism for the sustained activation of the HPA axis in the late-gestation ovine fetus?|
|Citation:||American Journal of Physiology-Endocrinology and Metabolism, 2002; 283(1 46-1):E165-E171|
|Publisher:||Amer Physiological Soc|
|Holloway AC, Howe DC, Chan G, Clifton VL, Smith R and Challis JR.|
|Abstract:||We hypothesized that urocortin might be produced in the pituitary of the late-gestation ovine fetus in a manner that could contribute to the regulation of ACTH output. We used in situ hybridization and immunohistochemistry to identify urocortin mRNA and protein in late-gestation fetal pituitary tissue. Levels of urocortin mRNA rose during late gestation and were associated temporally with rising concentrations of pituitary proopiomelanocortin (POMC) mRNA. Urocortin was localized both to cells expressing ACTH and to non-ACTH cells by use of dual immunofluorescence histochemistry. Transfection of pituitary cultures with urocortin antisense probe reduced ACTH output, whereas added urocortin stimulated ACTH output from cultured pituitary cells. Cortisol infusion for 96 h in chronically catheterized late-gestation fetal sheep significantly stimulated levels of pituitary urocortin mRNA. We conclude that urocortin is expressed in the ovine fetal pituitary and localizes with, and can stimulate output of, ACTH. Regulation of urocortin by cortisol suggests a mechanism to override negative feedback and sustain feedforward of fetal hypothalamic-pituitary-adrenal function, leading to birth|
|Keywords:||urocortin; ACTH; parturition; hypothalamo-pituitary-adrenal axis|
|Rights:||© 2002 by the American Physiological Society.|
|Appears in Collections:||Paediatrics publications|
Files in This Item:
There are no files associated with this item.
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.