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 Blood, 1 March 2008, Vol. 111, No. 5, pp. 2806-2815.
Prepublished online as a Blood First Edition Paper on December 3, 2007; DOI 10.1182/blood-2007-04-085555.

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NEOPLASIA

PAX2 expression by HHV-8–infected endothelial cells induced a proangiogenic and proinvasive phenotype

Valentina Fonsato1, Stefano Buttiglieri1, Maria Chiara Deregibus1, Benedetta Bussolati1, Elisabetta Caselli2, Dario Di Luca2, and Giovanni Camussi1

1 Department of Internal Medicine, Research Center for Experimental Medicine and Center for Molecular Biotechnology, University of Torino, Torino; and 2 Section of Microbiology, Department of Experimental and Diagnostic Medicine, University of Ferrara, Ferrara, Italy

In the present study, we evaluated whether infection of microvascular endothelial cells (HMECs) with HHV-8 can trigger the expression of PAX2 oncogene and whether PAX2 protein is involved in HHV-8–induced transformation of HMECs. We found that HHV-8 infection induced the expression of both the PAX2 gene and PAX2 protein in HMECs but failed to induce PAX2 protein in HMECs stably transfected with PAX2 antisense (HMEC-AS). HHV-8–infected HMECs but not HMEC-AS acquired proinvasive proadhesive properties, enhanced survival and in vitro angiogenesis, suggesting a correlation between PAX2 expression and the effects triggered by HHV-8 infection. When HMEC-expressing PAX2 by stable transfection with PAX2 sense gene or by HHV-8 infection were implanted in vivo in severe combined immunodeficient (SCID) mice, enhanced angiogenesis and proliferative lesions resembling KS were observed. HHV-8–infected HMEC-AS failed to induce angiogenesis and KS-like lesions. These results suggest that the expression of PAX2 is required for the proangiogenic and proinvasive changes induced by HHV-8 infection in HMECs. In conclusion, HHV-8 infection may activate an embryonic angiogenic program in HMECs by inducing the expression of PAX2 oncogene.


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