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 Blood, 15 October 2006, Vol. 108, No. 8, pp. 2624-2631.
Prepublished online as a Blood First Edition Paper on April 25, 2006; DOI 10.1182/blood-2005-12-007484.

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HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY

VEGF regulates the mobilization of VEGFR2/KDR from an intracellular endothelial storage compartment

Alexandra Gampel, Lara Moss, Matt C. Jones, Val Brunton, Jim C. Norman, and Harry Mellor

From the Mammalian Cell Biology Laboratory, Department of Biochemistry, School of Medical Sciences, University of Bristol, United Kingdom; and Beatson Institute for Cancer Research, Cancer Research UK, Beatson Laboratories, Glasgow, United Kingdom.

Endothelial cells respond to vascular endothelial growth factor (VEGF) to produce new blood vessels. This process of angiogenesis makes a critical contribution during embryogenesis and also in the response to ischemia in adult tissues. We have studied the intracellular trafficking of the major VEGF receptor KDR (VEGFR2). Unlike other related growth factor receptors, we find that a significant proportion of KDR is held in an endosomal storage pool within endothelial cells. We find that KDR can be delivered to the plasma membrane from this intracellular pool and that VEGF stimulates this recycling to the cell surface. KDR recycling appears to be distinct from the previously characterized Rab4- and Rab11-dependent pathways, but, instead, KDR+ recycling vesicles contain Src tyrosine kinase and VEGF-stimulated recycling requires Src activation. Taken together, these data show that intracellular trafficking of KDR is markedly different from other receptor tyrosine kinases and suggest that the regulation of KDR trafficking by VEGF provides a novel mechanism for controlling the sensitivity of endothelial cells to proangiogenic signals.


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Related Article in Blood Online:

VEGF calls its receptors from the recycling compartment
Yihai Cao
Blood 2006 108: 2506-2507. [Full Text] [PDF]





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