Migration of growth factor-stimulated epithelial and endothelial cells depends on EGFR transactivation by ADAM17

Thorsten Maretzky, Astrid Evers, Wenhui Zhou, Steven L. Swendeman, Pui-Mun Wong, Shahin Rafii, Karina Reiss and Carl P. Blobel ()
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Thorsten Maretzky: Arthritis and Tissue Degeneration Program, Hospital for Special Surgery at Weill Medical College, Cornell University, Caspary Research Building, 535 E 70th Street, New York, New York 10021, USA.
Astrid Evers: University Hospital Schleswig Holstein
Wenhui Zhou: Arthritis and Tissue Degeneration Program, Hospital for Special Surgery at Weill Medical College, Cornell University, Caspary Research Building, 535 E 70th Street, New York, New York 10021, USA.
Steven L. Swendeman: Arthritis and Tissue Degeneration Program, Hospital for Special Surgery at Weill Medical College, Cornell University, Caspary Research Building, 535 E 70th Street, New York, New York 10021, USA.
Pui-Mun Wong: Cell Biology and Genetics Program, Weill Medical College, Cornell University
Shahin Rafii: Cell Biology and Genetics Program, Weill Medical College, Cornell University
Karina Reiss: University Hospital Schleswig Holstein
Carl P. Blobel: Arthritis and Tissue Degeneration Program, Hospital for Special Surgery at Weill Medical College, Cornell University, Caspary Research Building, 535 E 70th Street, New York, New York 10021, USA.

Nature Communications, 2011, vol. 2, issue 1, 1-11

Abstract: Abstract The fibroblast growth factor receptor 2-IIIb (FGFR2b) and the vascular endothelial growth factor receptor 2 (VEGFR2) are tyrosine kinases that can promote cell migration and proliferation and have important roles in embryonic development and cancer. Here we show that FGF7/FGFR2b-dependent activation of epidermal growth factor receptor (EGFR)/ERK1/2 signalling and cell migration in epithelial cells require stimulation of the membrane-anchored metalloproteinase ADAM17 and release of heparin-binding epidermal growth factor (HB-EGF). Moreover, VEGF-A/VEGFR2-induced migration of human umbilical vein endothelial cells also depends on EGFR/ERK1/2 signalling and shedding of the ADAM17 substrate HB-EGF. The pathway used by the FGF7/FGFR2b signalling axis to stimulate shedding of substrates of ADAM17, including ligands of the EGFR, involves Src, p38 mitogen-activated protein-kinase and PI3K, but does not require the cytoplasmic domain of ADAM17. Based on these findings, ADAM17 emerges as a central component in a triple membrane-spanning pathway between FGFR2b or VEGFR2 and EGFR/ERK1/2 that is required for cell migration in keratinocytes and presumably also in endothelial cells.

Date: 2011
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DOI: 10.1038/ncomms1232

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