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

John S. Smith, Simon Kawa, Miles W. Cloyd, E. Brad Thompson

Research output: Contribution to journalArticle

9 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)1085-1091
Number of pages7
JournalEndocrinology
Volume133
Issue number3
DOIs
StatePublished - Sep 1993

ASJC Scopus subject areas

  • Endocrinology

Fingerprint Dive into the research topics of 'Interactions between human immunodeficiency virus infection and hormonal pathways: Enhancement of calcium-induced but reduction of glucocorticoid-induced cell death'. Together they form a unique fingerprint.

  • Cite this