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Blood, 15 January 2001, Vol. 97, No. 2, pp. 352-358
CHEMOKINES
HIV-1 Tat promotes monocyte chemoattractant protein-1 secretion
followed by transmigration of monocytes
In-Woo Park,
Jian-Feng Wang, and
Jerome E. Groopman
From the Division of Experimental Medicine and
Hematology/Oncology, Beth Israel Deaconess Medical Center, Harvard
Institutes of Medicine, Boston, MA.
The mechanism whereby HIV-infected cells transit from
the bloodstream into tissues is not well defined. This phenomenon was addressed by studying the effects of HIV-1 Tat, a protein secreted by
infected cells, on human lung microvascular endothelial cells (HMVEC-Ls). It was found that monocyte chemoattractant
protein-1 (MCP-1) was released from HMVEC-Ls in a dose- and
time-dependent manner after Tat treatment. MCP-1 is a potent
 -chemokine that recruits monocytes and T cells and promotes cell
adhesion and transmigration across an endothelial monolayer. It was
also observed that MCP-1 and the culture medium from Tat-treated
HMVEC-Ls were chemotactic for CD14+ monocytes
from human peripheral blood and for THP-1, a promonocytic cell line
used as a model system. To characterize the signaling pathways
underlying the observed induction of MCP-1, HMVEC-Ls were treated with
2 different protein kinase inhibitors: PD98059, a MAP kinase inhibitor,
and GF109203X, a protein kinase C (PKC) inhibitor. MCP-1 release was
significantly reduced when PKC was inhibited, and slightly decreased
when PI3 kinase was blocked; no effect on MCP-1 release was observed on
MAP kinase inhibition. Similarly, transmigration of THP-1 cells was
significantly impaired by the PKC inhibitor, but not by the other
tested inhibitors. These data indicate that the HIV-1 Tat protein may
act as a protocytokine by causing the release of MCP-1 from the
endothelial monolayer, and thereby facilitating monocyte transmigration
into tissues via a PKC signaling pathway.
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