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Vascular Endothelial Growth Factor Receptor-2–Induced Initial Endothelial Cell Migration Depends on the Presence of the Urokinase Receptor
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| Zeitschriftentitel: | Circulation Research |
|---|---|
| Personen und Körperschaften: | , , , , , , , |
| In: | Circulation Research, 94, 2004, 12, S. 1562-1570 |
| Format: | E-Article |
| Sprache: | Englisch |
| veröffentlicht: |
Ovid Technologies (Wolters Kluwer Health)
|
| Schlagwörter: |
| author_facet |
Prager, Gerald W. Breuss, Johannes M. Steurer, Stefan Olcaydu, Damla Mihaly, Judit Brunner, Patrick M. Stockinger, Hannes Binder, Bernd R. Prager, Gerald W. Breuss, Johannes M. Steurer, Stefan Olcaydu, Damla Mihaly, Judit Brunner, Patrick M. Stockinger, Hannes Binder, Bernd R. |
|---|---|
| author |
Prager, Gerald W. Breuss, Johannes M. Steurer, Stefan Olcaydu, Damla Mihaly, Judit Brunner, Patrick M. Stockinger, Hannes Binder, Bernd R. |
| spellingShingle |
Prager, Gerald W. Breuss, Johannes M. Steurer, Stefan Olcaydu, Damla Mihaly, Judit Brunner, Patrick M. Stockinger, Hannes Binder, Bernd R. Circulation Research Vascular Endothelial Growth Factor Receptor-2–Induced Initial Endothelial Cell Migration Depends on the Presence of the Urokinase Receptor Cardiology and Cardiovascular Medicine Physiology |
| author_sort |
prager, gerald w. |
| spelling |
Prager, Gerald W. Breuss, Johannes M. Steurer, Stefan Olcaydu, Damla Mihaly, Judit Brunner, Patrick M. Stockinger, Hannes Binder, Bernd R. 0009-7330 1524-4571 Ovid Technologies (Wolters Kluwer Health) Cardiology and Cardiovascular Medicine Physiology http://dx.doi.org/10.1161/01.res.0000131498.36194.6b <jats:p> The angiogenic response of endothelial cells initiated by different growth factors is accompanied by assembly of cell surface–bound proteolytic machinery as a prerequisite for focal invasion. We have shown previously how the vascular endothelial growth factor (VEGF) initiates proteolysis by activation of pro-urokinase (pro-PA) via the VEGF receptor-2 (VEGFR-2). We now show that the cell surface receptor of the uPA-system, the urokinase receptor (uPAR), is redistributed to focal adhesions at the leading edge of endothelial cells in response to VEGF. VEGF <jats:sub>165</jats:sub> and VEGF-E, both interacting with VEGFR-2, but not PlGF exclusively stimulating VEGFR-1, induce within minutes internalization of uPAR via an LDL receptor–like molecule, dependent on generation of active uPA and the presence of plasminogen activator inhibitor-1 (PAI-1). uPAR seems to play a pivotal role in VEGFR-2–induced endothelial cell migration because cleavage of surface uPAR impaired the migratory response of endothelial cells toward VEGF-E, but not toward PlGF. </jats:p> Vascular Endothelial Growth Factor Receptor-2–Induced Initial Endothelial Cell Migration Depends on the Presence of the Urokinase Receptor Circulation Research |
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| title |
Vascular Endothelial Growth Factor Receptor-2–Induced Initial Endothelial Cell Migration Depends on the Presence of the Urokinase Receptor |
| title_unstemmed |
Vascular Endothelial Growth Factor Receptor-2–Induced Initial Endothelial Cell Migration Depends on the Presence of the Urokinase Receptor |
| title_full |
Vascular Endothelial Growth Factor Receptor-2–Induced Initial Endothelial Cell Migration Depends on the Presence of the Urokinase Receptor |
| title_fullStr |
Vascular Endothelial Growth Factor Receptor-2–Induced Initial Endothelial Cell Migration Depends on the Presence of the Urokinase Receptor |
| title_full_unstemmed |
Vascular Endothelial Growth Factor Receptor-2–Induced Initial Endothelial Cell Migration Depends on the Presence of the Urokinase Receptor |
| title_short |
Vascular Endothelial Growth Factor Receptor-2–Induced Initial Endothelial Cell Migration Depends on the Presence of the Urokinase Receptor |
| title_sort |
vascular endothelial growth factor receptor-2–induced initial endothelial cell migration depends on the presence of the urokinase receptor |
| topic |
Cardiology and Cardiovascular Medicine Physiology |
| url |
http://dx.doi.org/10.1161/01.res.0000131498.36194.6b |
| publishDate |
2004 |
| physical |
1562-1570 |
| description |
<jats:p>
The angiogenic response of endothelial cells initiated by different growth factors is accompanied by assembly of cell surface–bound proteolytic machinery as a prerequisite for focal invasion. We have shown previously how the vascular endothelial growth factor (VEGF) initiates proteolysis by activation of pro-urokinase (pro-PA) via the VEGF receptor-2 (VEGFR-2). We now show that the cell surface receptor of the uPA-system, the urokinase receptor (uPAR), is redistributed to focal adhesions at the leading edge of endothelial cells in response to VEGF. VEGF
<jats:sub>165</jats:sub>
and VEGF-E, both interacting with VEGFR-2, but not PlGF exclusively stimulating VEGFR-1, induce within minutes internalization of uPAR via an LDL receptor–like molecule, dependent on generation of active uPA and the presence of plasminogen activator inhibitor-1 (PAI-1). uPAR seems to play a pivotal role in VEGFR-2–induced endothelial cell migration because cleavage of surface uPAR impaired the migratory response of endothelial cells toward VEGF-E, but not toward PlGF.
</jats:p> |
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| author | Prager, Gerald W., Breuss, Johannes M., Steurer, Stefan, Olcaydu, Damla, Mihaly, Judit, Brunner, Patrick M., Stockinger, Hannes, Binder, Bernd R. |
| author_facet | Prager, Gerald W., Breuss, Johannes M., Steurer, Stefan, Olcaydu, Damla, Mihaly, Judit, Brunner, Patrick M., Stockinger, Hannes, Binder, Bernd R., Prager, Gerald W., Breuss, Johannes M., Steurer, Stefan, Olcaydu, Damla, Mihaly, Judit, Brunner, Patrick M., Stockinger, Hannes, Binder, Bernd R. |
| author_sort | prager, gerald w. |
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| description | <jats:p> The angiogenic response of endothelial cells initiated by different growth factors is accompanied by assembly of cell surface–bound proteolytic machinery as a prerequisite for focal invasion. We have shown previously how the vascular endothelial growth factor (VEGF) initiates proteolysis by activation of pro-urokinase (pro-PA) via the VEGF receptor-2 (VEGFR-2). We now show that the cell surface receptor of the uPA-system, the urokinase receptor (uPAR), is redistributed to focal adhesions at the leading edge of endothelial cells in response to VEGF. VEGF <jats:sub>165</jats:sub> and VEGF-E, both interacting with VEGFR-2, but not PlGF exclusively stimulating VEGFR-1, induce within minutes internalization of uPAR via an LDL receptor–like molecule, dependent on generation of active uPA and the presence of plasminogen activator inhibitor-1 (PAI-1). uPAR seems to play a pivotal role in VEGFR-2–induced endothelial cell migration because cleavage of surface uPAR impaired the migratory response of endothelial cells toward VEGF-E, but not toward PlGF. </jats:p> |
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| spelling | Prager, Gerald W. Breuss, Johannes M. Steurer, Stefan Olcaydu, Damla Mihaly, Judit Brunner, Patrick M. Stockinger, Hannes Binder, Bernd R. 0009-7330 1524-4571 Ovid Technologies (Wolters Kluwer Health) Cardiology and Cardiovascular Medicine Physiology http://dx.doi.org/10.1161/01.res.0000131498.36194.6b <jats:p> The angiogenic response of endothelial cells initiated by different growth factors is accompanied by assembly of cell surface–bound proteolytic machinery as a prerequisite for focal invasion. We have shown previously how the vascular endothelial growth factor (VEGF) initiates proteolysis by activation of pro-urokinase (pro-PA) via the VEGF receptor-2 (VEGFR-2). We now show that the cell surface receptor of the uPA-system, the urokinase receptor (uPAR), is redistributed to focal adhesions at the leading edge of endothelial cells in response to VEGF. VEGF <jats:sub>165</jats:sub> and VEGF-E, both interacting with VEGFR-2, but not PlGF exclusively stimulating VEGFR-1, induce within minutes internalization of uPAR via an LDL receptor–like molecule, dependent on generation of active uPA and the presence of plasminogen activator inhibitor-1 (PAI-1). uPAR seems to play a pivotal role in VEGFR-2–induced endothelial cell migration because cleavage of surface uPAR impaired the migratory response of endothelial cells toward VEGF-E, but not toward PlGF. </jats:p> Vascular Endothelial Growth Factor Receptor-2–Induced Initial Endothelial Cell Migration Depends on the Presence of the Urokinase Receptor Circulation Research |
| spellingShingle | Prager, Gerald W., Breuss, Johannes M., Steurer, Stefan, Olcaydu, Damla, Mihaly, Judit, Brunner, Patrick M., Stockinger, Hannes, Binder, Bernd R., Circulation Research, Vascular Endothelial Growth Factor Receptor-2–Induced Initial Endothelial Cell Migration Depends on the Presence of the Urokinase Receptor, Cardiology and Cardiovascular Medicine, Physiology |
| title | Vascular Endothelial Growth Factor Receptor-2–Induced Initial Endothelial Cell Migration Depends on the Presence of the Urokinase Receptor |
| title_full | Vascular Endothelial Growth Factor Receptor-2–Induced Initial Endothelial Cell Migration Depends on the Presence of the Urokinase Receptor |
| title_fullStr | Vascular Endothelial Growth Factor Receptor-2–Induced Initial Endothelial Cell Migration Depends on the Presence of the Urokinase Receptor |
| title_full_unstemmed | Vascular Endothelial Growth Factor Receptor-2–Induced Initial Endothelial Cell Migration Depends on the Presence of the Urokinase Receptor |
| title_short | Vascular Endothelial Growth Factor Receptor-2–Induced Initial Endothelial Cell Migration Depends on the Presence of the Urokinase Receptor |
| title_sort | vascular endothelial growth factor receptor-2–induced initial endothelial cell migration depends on the presence of the urokinase receptor |
| title_unstemmed | Vascular Endothelial Growth Factor Receptor-2–Induced Initial Endothelial Cell Migration Depends on the Presence of the Urokinase Receptor |
| topic | Cardiology and Cardiovascular Medicine, Physiology |
| url | http://dx.doi.org/10.1161/01.res.0000131498.36194.6b |