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Enhanced natural-killer cell and erythropoietic activities in VEGF-A-overexpressing mice delay F-MuLU-induced erythroleukemia

David Cervi, Yuval Shaked, Mehran Haeri, Tatiana Usenko, Christina R Lee, Jody Haigh, Andras Nagy, Robert S Kerbel, Etan Yefenof and Yaacov Ben-David (2007) BLOOD. 109(5). p.2139-2146
abstract
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 (Vegf(hi/+)) were inoculated with F-MuLV. Unexpectedly, a significant delay in erythroleukemia was observed in Vegf(hi/+) mice when compared with wildtype controls. These results suggested an altered physiologic response arising from elevated VEGF-A levels that decelerated erythroleukemic progression. Characterization of hematopoiesis in Vegf(hi/+) spleens showed a higher natural killer cell activity, elevated B cells, and a decrease in T-cell number. Furthermore, higher erythroid progenitors (ie, CD34(+), CD36(+), and Teri119(+) cells) were evident in the bone marrow, spleen, and peripheral blood of Vegf(hi/+) mice. The CFU-E levels were significantly elevated in Vegf(hi/+) 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 Vegf(hi/+) mice, showed a delay in disease progression. We propose that a compensatory erythropoietic response combined with increased natural killer (NK) cell activity account for the extended. survival of erythroleukemic, Vegf(hi/+) mice.
Please use this url to cite or link to this publication:
author
organization
year
type
journalArticle (original)
publication status
published
subject
keyword
ENDOTHELIAL GROWTH-FACTOR, FRIEND-LEUKEMIA, BONE-MARROW, VIRUS, ANGIOGENESIS, GENE, FLI-1, IMMUNITY, DIFFERENTIATION, PROLIFERATION
journal title
BLOOD
Blood
volume
109
issue
5
pages
2139 - 2146
Web of Science type
Article
Web of Science id
000244641100055
JCR category
HEMATOLOGY
JCR impact factor
10.896 (2007)
JCR rank
2/61 (2007)
JCR quartile
1 (2007)
ISSN
0006-4971
DOI
10.1182/blood-2005.11-026823
language
English
UGent publication?
yes
classification
A1
copyright statement
I have transferred the copyright for this publication to the publisher
id
361939
handle
http://hdl.handle.net/1854/LU-361939
date created
2007-04-12 15:55:00
date last changed
2016-12-19 15:44:10
@article{361939,
  abstract     = {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 {\textacutedbl}hypermorphic{\textacutedbl} allele (Vegf(hi/+)) were inoculated with F-MuLV. Unexpectedly, a significant delay in erythroleukemia was observed in Vegf(hi/+) mice when compared with wildtype controls. These results suggested an altered physiologic response arising from elevated VEGF-A levels that decelerated erythroleukemic progression. Characterization of hematopoiesis in Vegf(hi/+) spleens showed a higher natural killer cell activity, elevated B cells, and a decrease in T-cell number. Furthermore, higher erythroid progenitors (ie, CD34(+), CD36(+), and Teri119(+) cells) were evident in the bone marrow, spleen, and peripheral blood of Vegf(hi/+) mice. The CFU-E levels were significantly elevated in Vegf(hi/+) 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 Vegf(hi/+) mice, showed a delay in disease progression. We propose that a compensatory erythropoietic response combined with increased natural killer (NK) cell activity account for the extended. survival of erythroleukemic, Vegf(hi/+) mice.},
  author       = {Cervi, David and Shaked, Yuval and Haeri, Mehran and Usenko, Tatiana and Lee, Christina R and Haigh, Jody and Nagy, Andras and Kerbel, Robert S and Yefenof, Etan and Ben-David, Yaacov},
  issn         = {0006-4971},
  journal      = {BLOOD},
  keyword      = {ENDOTHELIAL GROWTH-FACTOR,FRIEND-LEUKEMIA,BONE-MARROW,VIRUS,ANGIOGENESIS,GENE,FLI-1,IMMUNITY,DIFFERENTIATION,PROLIFERATION},
  language     = {eng},
  number       = {5},
  pages        = {2139--2146},
  title        = {Enhanced natural-killer cell and erythropoietic activities in VEGF-A-overexpressing mice delay F-MuLU-induced erythroleukemia},
  url          = {http://dx.doi.org/10.1182/blood-2005.11-026823},
  volume       = {109},
  year         = {2007},
}

Chicago
Cervi, David, Yuval Shaked, Mehran Haeri, Tatiana Usenko, Christina R Lee, Jody Haigh, Andras Nagy, Robert S Kerbel, Etan Yefenof, and Yaacov Ben-David. 2007. “Enhanced Natural-killer Cell and Erythropoietic Activities in VEGF-A-overexpressing Mice Delay F-MuLU-induced Erythroleukemia.” Blood 109 (5): 2139–2146.
APA
Cervi, D., Shaked, Y., Haeri, M., Usenko, T., Lee, C. R., Haigh, J., Nagy, A., et al. (2007). Enhanced natural-killer cell and erythropoietic activities in VEGF-A-overexpressing mice delay F-MuLU-induced erythroleukemia. BLOOD, 109(5), 2139–2146.
Vancouver
1.
Cervi D, Shaked Y, Haeri M, Usenko T, Lee CR, Haigh J, et al. Enhanced natural-killer cell and erythropoietic activities in VEGF-A-overexpressing mice delay F-MuLU-induced erythroleukemia. BLOOD. 2007;109(5):2139–46.
MLA
Cervi, David, Yuval Shaked, Mehran Haeri, et al. “Enhanced Natural-killer Cell and Erythropoietic Activities in VEGF-A-overexpressing Mice Delay F-MuLU-induced Erythroleukemia.” BLOOD 109.5 (2007): 2139–2146. Print.