help button home button Endocrine Society Endocrinology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
This version published online on February 17, 2005
Endocrinology, doi:10.1210/en.2004-1298
A more recent version of this article appeared on May 1, 2005
This Article
Right arrow Author Manuscript (PDF)
Right arrow All Versions of this Article:
146/5/2186    most recent
Author Manuscript (PDF)
Right arrow Purchase Article
Right arrow View Shopping Cart
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow Request Copyright Permission
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Soares, S. M.
Right arrow Articles by Chini, E. N.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Soares, S. M.
Right arrow Articles by Chini, E. N.

Submitted on October 4, 2004
Accepted on February 7, 2005

Role of the second messenger Cyclic-ADP-ribose on ACTH secretion from pituitary cells

Sandra M. Soares MD, Michael Thompson BS, and Eduardo N. Chini MD, PhD*

Departments of Anesthesiology, and Department of Physiology and Biophysics, Mayo Clinic, Rochester, Minnesota 55905

* To whom correspondence should be addressed. E-mail: Chini.eduardo{at}mayo.edu.

We examined the role of the second messenger cyclic-ADP-ribose (cADPR) on the regulation of ACTH secretion using AtT20 corticotroph tumor cell line. We found that the cADPR antagonist, 8-Br-cADPR, substantially diminished the secretion of ACTH induced by CRH (CRH) and potassium (KCl) in these cells, whereas Xestospongin C, an inositol 1,4,5-triphosphate receptor antagonist, had no effect. In addition, the cADPR agonist, 3-deaza-cADPR, augmented ACTH secretion. The presence of the components of the cADPR system namely: ryanodine receptor, CD38 and cADPR itself were determined in AtT20 cells. Furthermore, we observed that antagonists of the RyR and of the cADPR system can decrease the KCl induced Ca2+ transients in these cells. These results suggest that cADPR is a second messenger in pituitary cells and regulates ACTH secretion by a mechanism dependent on activation of the RyR by extracellular Ca2+.
Key words: cADPR • IP3 • endoplasmic reticulum • ryanodine channel






HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
Endocrinology Endocrine Reviews J. Clin. End. & Metab.
Molecular Endocrinology Recent Prog. Horm. Res. All Endocrine Journals
Copyright © 2005 by The Endocrine Society