Biphasic function of focal adhesion kinase in endothelial tube formation induced by fibril-forming collagens
| Autor: | Keishi Yamauchi, Masanori Yamazaki, Kiyoshi Hashizume, Satoshi Shigematsu, Teiji Takeda, Tomoko Kakizawa, Junko Nakamura |
|---|---|
| Rok vydání: | 2008 |
| Předmět: |
Angiogenesis
medicine.medical_treatment Integrin Biophysics Down-Regulation Neovascularization Physiologic Motility Biochemistry Collagen Type I Umbilical vein Focal adhesion Cell Movement medicine Animals Humans Collagen Type II Molecular Biology Cells Cultured Tube formation biology Growth factor Calpain Cell Biology Rats Cell biology Focal Adhesion Kinase 1 biology.protein Endothelium Vascular Gels |
| Zdroj: | Biochemical and Biophysical Research Communications. 374:699-703 |
| ISSN: | 0006-291X |
| DOI: | 10.1016/j.bbrc.2008.07.123 |
| Popis: | Migration and tube formation of endothelial cells are important in angiogenesis and require a coordinated response to the extra-cellular matrix (ECM) and growth factor. Since focal adhesion kinase (FAK) integrates signals from both ECM and growth factor, we investigated its role in angiogenesis. Type I and II collagens are fibril-forming collagens and stimulate human umbilical vein endothelial cells (HUVECs) to form tube structure. Although knockdown of FAK restrained cell motility and resulted in inhibition of tube formation, FAK degradation and tube formation occurred simultaneously after incubation with fibril-forming collagens. The compensation for the FAK degradation by a calpain inhibitor or transient over-expression of FAK resulted in disturbance of tube formation. These phenomena are specific to fibril-forming collagens and mediated via α2β1 integrin. In conclusion, our data indicate that FAK is functioning in cell migration, but fibril-forming collagen-induced FAK degradation is necessary for endothelial tube formation. |
| Databáze: | OpenAIRE |
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