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Blood, 1 June 2005, Vol. 105, No. 11, pp. 4516-4522.
Prepublished online as a Blood First Edition Paper on February 10, 2005; DOI 10.1182/blood-2004-09-3683.
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Submitted September 24, 2004
Accepted February 1, 2005
B-Raf dependent expression of vascular endothelial growth factor-A in Kaposi's sarcoma-associated herpesvirus infected human B cells
Shaw M Akula*, Patrick W Ford, Audy G Whitman, Khalief E Hamden, Benjaman A Bryan, Paul P Cook, and James A McCubrey
Department of Microbiology & Immunology, Brody School of Medicine, East Carolina University, Greenville, NC, USA
Department of Internal Medicine, Brody School of Medicine, East Carolina University, Greenville, NC, USA
* Corresponding author; email: akulas{at}mail.ecu.edu.
Kaposi's sarcoma-associated herpesvirus (KSHV/HHV-8) is etiologically linked to Kaposi's sarcoma (KS), primary effusion lymphoma (PEL), and multicentric Castleman disease. Vascular endothelial growth factor-A (VEGF-A) is one of the essential factors required in KSHV pathogenesis, mainly due to its ability to mediate angiogenesis. In this report, we analyzed the relationship between Raf and VEGF-A expression in KSHV infected hematopoietic cells. All of the KSHV infected cell lines (derived from PEL) expressed higher levels of B-Raf and VEGF-A when compared to uninfected cells. Inhibition of Raf > MEK > ERK signaling either by the use of MEK inhibitor (PD98059) or by siRNA specific to B-Raf, significantly lowered VEGF-A expression. In addition, B-Raf induced VEGF-A expression was demonstrated to be sufficient to enhance tubule formation in endothelial cells. Interestingly, we did not observe mutation in the B-Raf gene of the KSHV infected PEL cell lines. Taken together, we report for the first time, the ability of Raf associated signaling to play a role in the expression of VEGF-A in KSHV infected hematopoietic cells.
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