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Blood, 1 March 2007, Vol. 109, No. 5, pp. 2139-2146. Prepublished online as a Blood First Edition Paper on October 19, 2006; DOI 10.1182/blood-2005-11-026823. This Article Full Text (PDF) All Versions of this Article: blood-2005-11-026823v1 109/5/2139    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Cervi, D. Articles by Ben-David, Y. Search for Related Content PubMed PubMed Citation Articles by Cervi, D. Articles by Ben-David, Y. Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted November 10, 2005 Accepted October 10, 2006 Enhanced natural killer cell and erythropoietic activities in VEGF-A-overexpressing mice delay F-MuLV-induced erythroleukemia David Cervi, Yuval Shaked, Mehran Haeri, Tatiana Usenko, Christina R Lee, Jody J Haigh, Andras Nagy, Robert S Kerbel, Eitan Yefenof, and Yaacov Ben-David* Sunnybrook Health Sciences Centre, Canada Flanders Interuniversity Institute for Biotechnology (FIB), Ghent University, Belgium Samuel Lunenfeld Research Institute, Mount Sinai Hospital, Canada Lautenberg Center of Immunology, Hadassah Medical School, Israel * Corresponding author; email: bendavid{at}sri.utoronto.ca. We have previously reported that VEGF-A, in combination with MCP-5, contributes to leukemia progression within the splenic microenvironment of mice infected with F-MuLV. To study the influence of constitutively elevated VEGF-A levels on the progression of erythroleukemia, mice heterozygous for a VEGF-A "hypermorphic" allele (VEGFhi/+) were inoculated with F-MuLV. Unexpectedly, a significant delay in erythroleukemia was observed in VEGFhi/+ mice when compared to wild-type controls. These results suggested an altered physiological response arising from elevated VEGF-A levels that decelerated erythroleukemic progression. Characterization of hematopoiesis in VEGFhi/+ spleens showed a higher natural killer cell activity, elevated B-cells and a decrease in T-cell number. Furthermore, higher erythroid progenitors; i.e., CD34+, CD36+ and Ter119+ cells were evident in the bone marrow, spleen and peripheral blood of VEGFhi/+ mice. The CFU-E counts were significantly increased in VEGFhi/+ bone-marrow cultures and this elevation was blocked by a neutralizing antibody to VEGF-A receptor (VEGFR-2). Moreover, erythroleukemic mice were treated with recombinant erythropoietin and similar to diseased VEGFhi/+ mice, showed a delay in disease progression. We propose that a compensatory erythropoietic response combined with increased NK cell activity account for the extended survival of erythroleukemic, VEGFhi/+ mice. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: K. B. Harikumar, G. Kuttan, and R. Kuttan Inhibition of Viral Carcinogenesis by Phyllanthus amarus Integr Cancer Ther, September 1, 2009; 8(3): 254 - 260. [Abstract] [PDF]

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