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JCS ePress online publication date 22 Jan 2008
doi: 10.1242/jcs.022343


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Research Article

vFLIP from KSHV inhibits anoikis of primary endothelial cells


Sofia Efklidou, Ranbir Bailey, Nigel Field, Mahdad Noursadeghi, and Mary K. Collins*
* Author for correspondence (e-mail: mary.collins{at}ucl.ac.uk)

Kaposi's sarcoma-associated herpesvirus (KSHV or HHV-8) infection of endothelial cells is an early event in the aetiology of the endothelial cell tumour Kaposi's sarcoma (KS). We have examined the effect of the KSHV latent protein viral FLICE-like inhibitory protein (vFLIP) on dermal microvascular endothelial cell (MVEC) survival as vFLIP is expressed in the KSHV-infected cells within KS lesions. To do this, we have used a lentiviral vector to express vFLIP in MVECs in the absence of other KSHV proteins. vFLIP activates the classical NF-{kappa}B pathway in MVECs and causes nuclear translocation of RelA/p65. This NF-{kappa}B activation prevents detachment-induced apoptosis (anoikis) of MVECs but does not inhibit apoptosis induced by removal of essential survival factors, including vascular endothelial growth factor (VEGF). vFLIP expression inhibits anoikis in part by inducing the secretion of an additional paracrine survival factor(s). The implications of these results for KS development are discussed.







© The Company of Biologists Ltd 2008