Multi-physics interactions drive VEGFR2 relocation on endothelial cells
| Autor: | Stefania Mitola, Cosetta Ravelli, Alberto Salvadori, Gian Paolo Beretta, Valentina Damioli |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2017 |
| Předmět: |
0301 basic medicine
Models Molecular lcsh:Medicine Ligands Article Cell Line Cell membrane Extracellular matrix 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine medicine Animals lcsh:Science Receptor Multidisciplinary lcsh:R Cell Membrane Fluorescence recovery after photobleaching Endothelial Cells Kinase insert domain receptor Vascular Endothelial Growth Factor Receptor-2 Vascular endothelial growth factor 030104 developmental biology Membrane medicine.anatomical_structure chemistry Cell culture 030220 oncology & carcinogenesis Biophysics lcsh:Q Cattle Fluorescence Recovery After Photobleaching |
| Zdroj: | Scientific Reports Scientific Reports, Vol 7, Iss 1, Pp 1-11 (2017) |
| ISSN: | 2045-2322 |
| Popis: | Vascular Endothelial Growth Factor Receptor-2 (VEGFR2) is a pro-angiogenic receptor, expressed on endothelial cells (ECs). Although biochemical pathways that follow the VEGFR2 activation are well established, knowledge about the dynamics of receptors on the plasma membrane remains limited. Ligand stimulation induces the polarization of ECs and the relocation of VEGFR2, either in cell protrusions or in the basal aspect in cells plated on ligand-enriched extracellular matrix (ECM). We develop a mathematical model in order to simulate the relocation of VEGFR2 on the cell membrane during the mechanical adhesion of cells onto a ligand-enriched substrate. Co-designing the in vitro experiments with the simulations allows identifying three phases of the receptor dynamics, which are controlled respectively by the high chemical reaction rate, by the mechanical deformation rate, and by the diffusion of free receptors on the membrane. The identification of the laws that regulate receptor polarization opens new perspectives toward developing innovative anti-angiogenic strategies through the modulation of EC activation. |
| Databáze: | OpenAIRE |
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