Journal
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH
Volume 1793, Issue 8, Pages 1366-1371Publisher
ELSEVIER
DOI: 10.1016/j.bbamcr.2009.05.007
Keywords
HIV; Opioid; beta-arrestin; gp120; Drug use; Lymphocyte; Apoptosis
Categories
Funding
- National Institutes of Health [DA020120]
- East Tennessee State University Research Development Committee (ETSU RDC) [2-25491, 06-002M]
- Rajajohns Hopkins University School of Medicine
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The mechanisms by which opioids affect progression of human immunodeficiency virus type 1 (HIV-1) infection are not well-defined. HIV-1 gp120 is important in the apoptotic death of uninfected, bystander T cells. In this study, we show that co-treatment of human peripheral blood mononuclear cells (PBMC) with HIV-1 gp120/morphine synergistically induces apoptosis in PBMC. Co-treatment of murine splenocytes from mu opiate receptor knockout mice with gp120/morphine resulted in decreased apoptosis when compared to splenocytes from wild type mice. Co-treatment of human PBMC or murine splenocytes with gp120/morphine led to decreased expression of beta-arrestin 2, a protein required for opioid-mediated signaling. The role of beta-arrestin 2 was confirmed in Jurkat lymphocytes, in which 1) over-expression of beta-arrestin 2 inhibited gp120/morphine-induced apoptosis and 2) RNA interference of beta-arrestin 2 expression enhanced gp120/morphine-induced apoptosis. These data suggest a novel mechanism by which HIV-1 gp120 and opioids induce lymphocyte cell death. (C) 2009 Elsevier B.V. All rights reserved.
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