help button home button Endocrine Society JCEM JCEM Call for Nominations for EIC
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
This Article
Right arrow Submit a related Letter to the Editor
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
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 HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Manolagas, S. C.
Right arrow Articles by Deftos, L. J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Manolagas, S. C.
Right arrow Articles by Deftos, L. J.

Journal of Clinical Endocrinology & Metabolism, Vol 63, 394-400, Copyright © 1986 by Endocrine Society

ARTICLES

The antiproliferative effect of calcitriol on human peripheral blood mononuclear cells

SC Manolagas, DM Provvedini, EJ Murray, CD Tsoukas and LJ Deftos

Activation of lymphocytes leads to the expression of receptors for the calcitropic hormone calcitriol [1,25(OH)2D3], and calcitriol is a potent inhibitor of interleukin-2 (IL-2) and of lymphocyte proliferation. We used peripheral blood mononuclear cells (PBM) activated in vitro with phytohemagglutinin to study 1) the relationship between 1,25(OH)2D3 receptor expression, IL-2 production, and 1,25(OH)2D3-induced inhibition of PBM proliferation in connection with the cell cycle; 2) the effect of 1,25(OH)2D3 on PBM activation and on the expression of activation-related molecules including the IL-2 receptor, and 3) the role of calcium in the antiproliferative effect of the hormone. 1,25(OH)2D3 receptor expression occurred when PBM entered the G1a phase of the cell cycle. The concentration of the receptor protein reached a peak at G1b and declined during the S phase. 1,25(OH)2D3 inhibited cell proliferation by blocking PBM at the G1a-G1b border. The antiproliferative effect of calcitriol was not caused by hormonal interference with the calcium-dependent activation process nor with the expression of activation-related molecules including the IL-2 receptor. Moreover, this effect was not influenced by extracellular calcium, suggesting that the hormonal action cannot be due to calcium translocation. These findings support the contention that 1,25(OH)2D3- induced inhibition of PBM proliferation is mediated through selective inhibition of IL-2 production.


This article has been cited by other articles:


Home page
 Arch OphthalmolHome page
N. Parekh, R. J. Chappell, A. E. Millen, D. M. Albert, and J. A. Mares
Association Between Vitamin D and Age-Related Macular Degeneration in the Third National Health and Nutrition Examination Survey, 1988 Through 1994
Arch Ophthalmol, May 1, 2007; 125(5): 661 - 669.
[Abstract] [Full Text] [PDF]

Home page
 EndocrinologyHome page
J. W. Morgan, D. J. Sliney, D. M. Morgan, and A. L. Maizel
Differential Regulation of Gene Transcription in Subpopulations of Human B Lymphocytes by Vitamin D3
Endocrinology, January 1, 1999; 140(1): 381 - 391.
[Abstract] [Full Text]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Endocrinology Endocrine Reviews J. Clin. End. & Metab.
Molecular Endocrinology Recent Prog. Horm. Res. All Endocrine Journals
Copyright © 1986 by The Endocrine Society