Suppressive effects of vascular endothelial growth factor-B on tumor growth in a mouse model of pancreatic neuroendocrine tumorigenesis.
<h4>Background</h4>The family of vascular endothelial growth factors (VEGF) contains key regulators of blood and lymph vessel development, including VEGF-A, -B, -C, -D, and placental growth factor. The role of VEGF-B during physiological or pathological angiogenesis has not yet been conc...
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2010
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oai:doaj.org-article:fa5b3c2c3fb94973ad79dd3b3be2ade12021-11-18T07:36:32ZSuppressive effects of vascular endothelial growth factor-B on tumor growth in a mouse model of pancreatic neuroendocrine tumorigenesis.1932-620310.1371/journal.pone.0014109https://doaj.org/article/fa5b3c2c3fb94973ad79dd3b3be2ade12010-11-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/21124841/?tool=EBIhttps://doaj.org/toc/1932-6203<h4>Background</h4>The family of vascular endothelial growth factors (VEGF) contains key regulators of blood and lymph vessel development, including VEGF-A, -B, -C, -D, and placental growth factor. The role of VEGF-B during physiological or pathological angiogenesis has not yet been conclusively delineated. Herein, we investigate the function of VEGF-B by the generation of mouse models of cancer with transgenic expression of VEGF-B or homozygous deletion of Vegfb.<h4>Methodology/principal findings</h4>Ectopic expression of VEGF-B in the insulin-producing β-cells of the pancreas did not alter the abundance or architecture of the islets of Langerhans. The vasculature from transgenic mice exhibited a dilated morphology, but was of similar density as that of wildtype mice. Unexpectedly, we found that transgenic expression of VEGF-B in the RIP1-Tag2 mouse model of pancreatic neuroendocrine tumorigenesis retarded tumor growth. Conversely, RIP1-Tag2 mice deficient for Vegfb presented with larger tumors. No differences in vascular density, perfusion or immune cell infiltration upon altered Vegfb gene dosage were noted. However, VEGF-B acted to increase blood vessel diameter both in normal pancreatic islets and in RIP1-Tag2 tumors.<h4>Conclusions/significance</h4>Taken together, our results illustrate the differences in biological function between members of the VEGF family, and highlight the necessity of in-depth functional studies of VEGF-B to fully understand the effects of VEGFR-1 inhibitors currently used in the clinic.Imke AlbrechtLucie KopfsteinKarin StrittmatterTibor SchomberAnnelie FalkevallCarolina E HagbergPascal LorentzMichael JeltschKari AlitaloUlf ErikssonGerhard ChristoforiKristian PietrasPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 5, Iss 11, p e14109 (2010) |
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Medicine R Science Q Imke Albrecht Lucie Kopfstein Karin Strittmatter Tibor Schomber Annelie Falkevall Carolina E Hagberg Pascal Lorentz Michael Jeltsch Kari Alitalo Ulf Eriksson Gerhard Christofori Kristian Pietras Suppressive effects of vascular endothelial growth factor-B on tumor growth in a mouse model of pancreatic neuroendocrine tumorigenesis. |
| description |
<h4>Background</h4>The family of vascular endothelial growth factors (VEGF) contains key regulators of blood and lymph vessel development, including VEGF-A, -B, -C, -D, and placental growth factor. The role of VEGF-B during physiological or pathological angiogenesis has not yet been conclusively delineated. Herein, we investigate the function of VEGF-B by the generation of mouse models of cancer with transgenic expression of VEGF-B or homozygous deletion of Vegfb.<h4>Methodology/principal findings</h4>Ectopic expression of VEGF-B in the insulin-producing β-cells of the pancreas did not alter the abundance or architecture of the islets of Langerhans. The vasculature from transgenic mice exhibited a dilated morphology, but was of similar density as that of wildtype mice. Unexpectedly, we found that transgenic expression of VEGF-B in the RIP1-Tag2 mouse model of pancreatic neuroendocrine tumorigenesis retarded tumor growth. Conversely, RIP1-Tag2 mice deficient for Vegfb presented with larger tumors. No differences in vascular density, perfusion or immune cell infiltration upon altered Vegfb gene dosage were noted. However, VEGF-B acted to increase blood vessel diameter both in normal pancreatic islets and in RIP1-Tag2 tumors.<h4>Conclusions/significance</h4>Taken together, our results illustrate the differences in biological function between members of the VEGF family, and highlight the necessity of in-depth functional studies of VEGF-B to fully understand the effects of VEGFR-1 inhibitors currently used in the clinic. |
| format |
article |
| author |
Imke Albrecht Lucie Kopfstein Karin Strittmatter Tibor Schomber Annelie Falkevall Carolina E Hagberg Pascal Lorentz Michael Jeltsch Kari Alitalo Ulf Eriksson Gerhard Christofori Kristian Pietras |
| author_facet |
Imke Albrecht Lucie Kopfstein Karin Strittmatter Tibor Schomber Annelie Falkevall Carolina E Hagberg Pascal Lorentz Michael Jeltsch Kari Alitalo Ulf Eriksson Gerhard Christofori Kristian Pietras |
| author_sort |
Imke Albrecht |
| title |
Suppressive effects of vascular endothelial growth factor-B on tumor growth in a mouse model of pancreatic neuroendocrine tumorigenesis. |
| title_short |
Suppressive effects of vascular endothelial growth factor-B on tumor growth in a mouse model of pancreatic neuroendocrine tumorigenesis. |
| title_full |
Suppressive effects of vascular endothelial growth factor-B on tumor growth in a mouse model of pancreatic neuroendocrine tumorigenesis. |
| title_fullStr |
Suppressive effects of vascular endothelial growth factor-B on tumor growth in a mouse model of pancreatic neuroendocrine tumorigenesis. |
| title_full_unstemmed |
Suppressive effects of vascular endothelial growth factor-B on tumor growth in a mouse model of pancreatic neuroendocrine tumorigenesis. |
| title_sort |
suppressive effects of vascular endothelial growth factor-b on tumor growth in a mouse model of pancreatic neuroendocrine tumorigenesis. |
| publisher |
Public Library of Science (PLoS) |
| publishDate |
2010 |
| url |
https://doaj.org/article/fa5b3c2c3fb94973ad79dd3b3be2ade1 |
| work_keys_str_mv |
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| _version_ |
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