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From the Cattedra di Nefrologia,*
Dipartimento di
Medicina Interna, Università di Torino, Torino; the Istituto
Nazionale per la Ricerca sul Cancro,
Genova;
and the Cattedra di Microbiologia,
Dipartimento di Scienze Cliniche e Biologiche, Università
dell’Insubria, Varese, Italy
In the present study, we evaluated whether
motility of Kaposi’s sarcoma (KS) spindle cells induced by HIV-1 Tat
protein is dependent on the synthesis of platelet-activating factor
(PAF). The results obtained indicate that Tat induced a dose-dependent
synthesis of PAF from KS cells at a concentration as low as 0.1 ng/ml.
PAF production started rapidly after Tat stimulation, peaking
at 30 minutes and declining thereafter. Tat-induced cell migration was
also a rapid event starting at 30 minutes. The motility was abrogated
by addition of a panel of chemically unrelated PAF receptor antagonists
(WEB 2170, CV 3988, CV 6209, and BN
52021), suggesting that the synthesized PAF mediates the
motogenic effect of Tat. This effect was also present on cells plated
on a type-I collagen-, fibronectin-, or basement
membrane extract-coated surface. Expression of PAF receptor-specific
mRNA was detected in KS cells. In addition, examination of the
cytoskeletal organization showed that Tat-mediated KS cell
redistribution of actin filaments and shape change was also inhibited
by a PAF receptor antagonist. Moreover, PAF receptor blockade
prevented the up-regulation of ß1 integrin and the down-regulation of
vß3 observed after stimulation of KS cells with Tat. In
conclusion, the results of the present study indicate that
Tat-induced PAF synthesis plays a critical role in triggering the
events involved in motility of KS cells.
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