Efklidou, S and Bailey, R and Field, N and Noursadeghi, M and Collins, MK (2008) vFLIP from KSHV inhibits anoikis of primary endothelial cells. J CELL SCI , 121 (4) 450 - 457. 10.1242/jcs.022343.
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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.
|Title:||vFLIP from KSHV inhibits anoikis of primary endothelial cells|
|Keywords:||vFLIP, anoikis, NF-kappa B, endothelial cell, SARCOMA-ASSOCIATED HERPESVIRUS, NF-KAPPA-B, PRIMARY EFFUSION LYMPHOMA, GROWTH-FACTOR RECEPTOR-3, KAPOSIS-SARCOMA, GENE-EXPRESSION, SPINDLE CELLS, LYMPHATIC ENDOTHELIUM, CHEMOKINE PRODUCTION, TRANSFORMED-CELLS|
|UCL classification:||UCL > School of Life and Medical Sciences > Faculty of Life Sciences > Biosciences (Division of) > Neuroscience, Physiology and Pharmacology|
UCL > School of Life and Medical Sciences > Faculty of Medical Sciences > Infection and Immunity (Division of) > Research Department of Immunology
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