help button home button Endocrine Society Endocrinology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
This Article
Right arrow Full Text (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 HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Smith, J. S.
Right arrow Articles by Thompson, E. B.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Smith, J. S.
Right arrow Articles by Thompson, E. B.

Endocrinology, Vol 133, 1085-1091, Copyright © 1993 by Endocrine Society

ARTICLES

Interactions between human immunodeficiency virus infection and hormonal pathways: enhancement of calcium-induced but reduction of glucocorticoid-induced cell death

JS Smith, S Kawa, MW Cloyd and EB Thompson
University of Texas Medical Branch, Department of Human Biological Chemistry and Genetics, Galveston 77555-0645.

We examined the effect of chronic human immunodeficiency virus 1 (HIV- 1) infection on the growth of human leukemic CEM T cells exposed to compounds which act through several major hormone or hormone-like signal transduction systems. Three were not altered by HIV-1 infection. Micromolar 8-bromo-cAMP inhibited cell growth equally in uninfected and infected cells. At the concentrations tested, neither (Bu)2cAMP nor the stimulator of protein kinase C, phorbol 12-myristate 13-acetate, altered the growth of infected or uninfected cells. The synthetic prostaglandin analog enisoprost also inhibited both equally. However, responses to two basic signal transduction systems, calcium uptake and the glucocorticoid pathway, were influenced by HIV infection. In chronically HIV-infected cells increased sensitivity to lysis by the calcium ionophore A23187 was observed. Additionally, the infected cells contained reduced amounts of glucocorticoid receptor sites and showed a statistically significant shift toward resistance to glucocorticoid- induced apoptosis.


This article has been cited by other articles:


Home page
 J. Biol. Chem.Home page
N. Ismaili, R. Blind, and M. J. Garabedian
Stabilization of the Unliganded Glucocorticoid Receptor by TSG101
J. Biol. Chem., March 25, 2005; 280(12): 11120 - 11126.
[Abstract] [Full Text] [PDF]

Home page
 BloodHome page
R. Ogawa, M. B. Streiff, A. Bugayenko, and G. J. Kato
Inhibition of PDE4 phosphodiesterase activity induces growth suppression, apoptosis, glucocorticoid sensitivity, p53, and p21WAF1/CIP1 proteins in human acute lymphoblastic leukemia cells
Blood, May 1, 2002; 99(9): 3390 - 3397.
[Abstract] [Full Text] [PDF]

Home page
 Ann. N. Y. Acad. Sci.Home page
G. NORBIATO, M. BEVILACQUA, T. VAGO, and M. CLERICI
Glucocorticoid Resistance and the Immune Function in the Immunodeficiency Syndrome
Ann. N.Y. Acad. Sci., May 1, 1998; 840(1): 835 - 847.
[Abstract] [Full Text] [PDF]


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 © 1993 by The Endocrine Society