Urokinase plasminogen activator receptor (uPAR; CD87) expression on monocytic cells and T cells is modulated by HIV-1 infection.

The transmembranous urokinase-type plasminogen activator receptor (uPAR; CD87) focuses the formation of active plasmin at the cell surface, thus enhancing directional extracellular proteolysis. Since proteolysis is involved in processes like adhesion, chemotaxis and migration which are important for viral spreading, we investigated the expression of uPAR in HIV-infected cells. Expression of CD87 was upmodulated in U937 monocytic cells as well as in the T cell line H9 and in peripheral blood mononuclear cells (PBMC), both on protein and on mRNA level. This upmodulation was not caused by enhanced mRNA stability but by an enhanced transcriptional rate of the CD87 gene as shown by nuclear run-on analysis. To identify the HIV-responsive element in the CD87 promoter we investigated the promoter activity in U937 and H9 cells at different time points after HIV-infection. Although the transcription of the CD87 gene is higher in HIV-infected cells the promoter activity declines after infection, indicating the presence of an additional regulatory element located upstream of the known promoter sequence or in intron sequences.