Abstract
The normal function of the endothelium is impaired in HIV-1 infection. Disturbances of the local cytokines as well as the release of HIV-1 Tat by infected mononuclear cells play a role in endothelial dysfunction. We studied the effects of Tat on the human endothelial ECV cell line. In this system, Tat inhibited cell proliferation only in the presence of fibronectin as a culture substrate, whereas it did not modulate plasminogen activator activity, cell migration, or synthesis of fibronectin. Because amino acids 49-57 contains a nuclear translocation sequence, we also evaluated the potential intracellular role of Tat in tat-transfected ECV cells. tat transfectants showed inhibition of cell growth, unaffected cell migration and plasminogen activator activity, and a significant induction of the expression of fibronectin.
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