Deletion of vascular endothelial growth factor in myeloid cells accelerates tumorigenesis

Christian Stockmann, Andrew Doedens, Alexander Weidemann, Na Zhang, Norihiko Takeda, Joshua I. Greenberg, David A. Cheresh and Randall S. Johnson ()
Additional contact information
Christian Stockmann: Molecular Biology Section
Andrew Doedens: Molecular Biology Section
Alexander Weidemann: Molecular Biology Section
Na Zhang: Molecular Biology Section
Norihiko Takeda: Molecular Biology Section
Joshua I. Greenberg: and
David A. Cheresh: University of California, San Diego, San Diego, California 92093, USA
Randall S. Johnson: Molecular Biology Section

Nature, 2008, vol. 456, issue 7223, 814-818

Abstract: Angoiogenesis and tumorigenesis: mixed messages from VEGF VEGF (vascular endothelial growth factor) is an important angiogenic factor that has been implicated in tumorigenesis. Two papers now show that the function of VEGF is far more complex, as VEFG can negatively regulate angiogenesis and limit tumorigenesis. In one study, Greenberg et al. found that VEGF can inhibit angiogenesis, by impeding the function of the PDGF (platelet-derived growth factor) receptor on pericytes, leading to a loss of pericyte coverage of blood vessels. This involves the formation of heterodimers between the receptors for VEGF and PDGF. In another paper, Stockmann et al. deleted VEGF production in myeloid cells, but not other cell types. Unexpectedly, they found more rapid tumour development in these mice, at the same time as attenuated tumour vascularization and the formation of morphologically and functionally normalized blood vessels. In contrast, tumours lacking VEGF altogether grew more slowly.

Date: 2008
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DOI: 10.1038/nature07445

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