HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Huber, P. Articles by Vilgrain, I. Search for Related Content PubMed PubMed Citation Articles by Huber, P. Articles by Vilgrain, I.

Laboratoire Développement et Vieillissement de l’Endothelium, INSERM EMI 02-19, DRDC/DVE, CEA-Grenoble, 17 rue des Martyrs, 38054 Grenoble, Cedex 9, France
¹ INSERM EMI 01-05, Department of Cellular Responses and Dynamics, CEA, Grenoble, France

(Requests for offprints should be addressed to I Vilgrain; Email: ivilgrain{at}cea.fr)

Vascular endothelial-cadherin (VE-cadherin) is an endothelial cell-specific adhesion protein that is localised at cell–cell contacts. This molecule is an important determinant of vascular architecture and endothelial cell survival. In the adrenal cortex, steroidogenic and endothelial cells form a complex architecture. The adrenocorticotrophin hormone (ACTH) regulates gland homeostasis whose secretion is subjected to a negative feedback by adrenocorticosteroids. The aim of the present study was to determine whether VE-cadherin expression in the adrenal gland was regulated by hormonal challenge. We demonstrated that VE-cadherin protein levels were dramatically decreased (23.5 ± 3.7%) by dexamethasone injections in the mouse and were restored by ACTH within 7 days (94.9 ± 18.6%). Flow cytometry analysis of adrenal cells showed that the ratios of endothelial versus total adrenal cells were identical (35%) in dexamethasone- or ACTH-treated or untreated mice, suggesting that VE-cadherin expression could be regulated by ACTH. We demonstrate the existence of a transcriptional regulation of the VE-cadherin gene using transgenic mice carrying the chloramphenicol acetyl transferase gene under the control of the VE-cadherin promoter. Indeed, the promoter activity in the adrenals, but not in the lung or liver, was decreased in response to dexamethasone treatment (40 ± 1.3%) and was partially restored after gland regeneration by ACTH injection (82 ± 3%). In conclusion, our results show that transcription of a specific endothelial gene is controlled by the hypothalamo–pituitary axis and the data expand the knowledge regarding the role of ACTH in the regulation of the adrenal vascular network.

This article has been cited by other articles:

				P. Martins, F. Schmitt, H. Almeida, and J. M. Frazao Evaluation of parathyroid gland angiogenesis in chronic kidney disease associated with secondary hyperparathyroidism Nephrol. Dial. Transplant., September 1, 2008; 23(9): 2889 - 2894. [Abstract] [Full Text] [PDF]

				D. X. Zhang, K. M. Gauthier, J. R. Falck, A. Siddam, and W. B. Campbell Steroid-Producing Cells Regulate Arterial Tone of Adrenal Cortical Arteries Endocrinology, August 1, 2007; 148(8): 3569 - 3576. [Abstract] [Full Text] [PDF]

				H.-C. Lam, S.-M. Kuo, M.-J. Chuang, H.-M. Keng, P.-R. Lin, G.-S. Liu, C.-M. Hsu, S.-L. Howng, and M.-H. Tai Blockade of endothelin-1 release contributes to the anti-angiogenic effect by pro-opiomelanocortin overexpression in endothelial cells. Experimental Biology and Medicine, June 1, 2006; 231(6): 782 - 788. [Abstract] [Full Text] [PDF]