VE-cadherin increases the half-life of VEGF receptor 2

Experimental Cell Research
Mónica R CaleraAndrius Kazlauskas

Abstract

VE-cadherin plays a critical role in cell-cell interactions by forming adherens junctions in endothelial cells. VE-cadherin has increasingly been implicated in the cell signaling cascades initiated by the activation of growth factor receptors. Vascular endothelial growth factor receptor 2 (VEGFR-2) is present in regions of cell-cell contact and coimmunoprecipitates with VE-cadherin. In this study, we report that stable overexpression of VE-cadherin in two different endothelial cells induced an increase in VEGFR-2 protein levels. The increase in VEGFR-2 was also induced by overexpression of other classical cadherins such as E-cadherin or N-cadherin. Removing the extracellular domain of VE-cadherin abolished this effect, and a truncated form of VE-cadherin lacking the intracellular domain decreased VEGFR-2 instead of increasing it. VE-cadherin-induced changes in VEGFR-2 levels were paralleled by a corresponding shift in the VEGF-dependent activation of MAPK signaling, which demonstrated the functional relevance of varying the VEGFR-2 levels. Since VE-cadherin upregulated endogenous VEGFR-2 or exogenously expressed VEGFR-2, we hypothesized that the mechanism may be posttranslational. Indeed, the half-life of VEGFR-2 was 70 min in ...Continue Reading

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