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The human immunodeficiency virus type-1 Tat protein upregulates Bcl-2 gene
expression in Jurkat T-cell lines and primary peripheral blood mononuclear
cells
G Zauli, D Gibellini, A Caputo, A Bassini, M Negrini, M Monne, M Mazzoni and S Capitani
Institute of Human Anatomy, University of Ferrara, Italy.
The regulatory Tat protein of human immunodeficiency virus type-1 (HIV- 1)
exerts a pleyotropic activity on the survival and proliferation of
different cell types in culture. In this report, we investigated the effect
of either endogenous or exogenous Tat on Bcl-2 proto-oncogene expression
and cell survival in Jurkat T-cell lines and primary peripheral blood
mononuclear cells. Stable and transient transfections of Jurkat cells with
the cDNA of tat and a plasmid containing Bcl-2 promoter in front of CAT
(Bcl-2 Pr/CAT) stimulated CAT activity and showed an increase of Bcl-2 mRNA
and protein expression. This effect was specifically related to tat,
because Jurkat cells transfected with the cDNA of tat in antisense
orientation, tat carrying a mutation in the amino acid cys22-gly22, or the
control vector alone (pRPneo-SL3) did not show any significant difference
in Bcl-2 promoter activity with respect to parental Jurkat cells. We also
observed a specific correlation between tat-induced Bcl-2 gene expression
and inhibition of apoptosis induced by serum withdrawal. Our results
suggest that the structural integrity of the activation domain of Tat was
required for the promotion of the Bcl-2 promoter and Jurkat cell survival,
because a single mutation in the aminoacid cys22 was sufficient to
completely block the upregulation of Bcl-2 and inhibition of apoptosis.
Moreover, picomolar concentrations of native or recombinant Tat were able
to upregulate Bcl-2 expression both in Jurkat and primary peripheral blood
mononuclear cells, suggesting that extracellular Tat, actively released by
infected cells, may also play a significant role in suppressing apoptosis.
An aberrant cell survival of lymphoid cells consequent to the upregulation
of Bcl-2 may represent an additional pathogenetic mechanism that could help
explain both the dysregulated immune response and the frequent occurrence
of hyperplastic/neoplastic disorders in HIV- 1-seropositive individuals.
Volume 86,
Issue 10,
pp. 3823-3834,
11/15/1995
Copyright © 1995 by The American Society of Hematology
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