Nucleic Acids Research, Vol 27, Issue 16 3291-3299, Copyright © 1999 by Oxford University Press
O Rohr, BE Sawaya, D Lecestre, D Aunis and E Schaeffer
Recent studies have reported that lymphocytes produce, transport and bind
dopamine present in plasma. However, the action of dopamine on HIV- 1 gene
expression in cells of the immune system has not yet been examined. Here,
we have investigated the regulation of HIV-1 expression by dopamine in
Jurkat T cells and in primary blood mononuclear cells (PBMC). HIV-1
replication was increased by dopamine, which correlated with the increased
levels of HIV-1 transactivation. Our transient expression data revealed
that dopamine stimulated transcription through the NF-kappaB element
present in the long terminal repeat. The importance of NF-kappaB sites was
confirmed by using vectors containing wild-type or mutant kappaB sites in a
heterologous promoter. Consistent with the role of NF-kappaB in mediating
dopamine responsiveness, the proteasome inhibitor MG132 abolished
dopamine-induced transcriptional activation. We further explored the effect
of dopamine in the presence of phorbol esters or tumor necrosis
factor-alpha (TNF-alpha) known to activate NF-kappaB. The combination of
dopamine and TNF-alpha led to a stimulation of HIV-1 transcription and
replication. However, in contrast with TNF-alpha, dopamine treatment did
not affect NF-kappaB DNA binding activity nor the concentrations of p50,
p65 and IkappaB- alpha proteins, which suggests a distinct NF-kappaB
activation mechanism. These results reveal a new link between the dopamine
system, cytokine signaling pathway and regulation of gene expression via
the involvement of NF-kappaB in T cells and PBMC.
ARTICLES
Dopamine stimulates expression of the human immunodeficiency virus type 1 via NF-kappaB in cells of the immune system
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