Abstract
Sphingosine-1-phosphate (S1P) induces capillary formation of endothelial cells on Matrigel in accompany with actin assembly and accumulation of cortactin and Arp2/3 complex at the cell-leading edge. Suppression of cortactin expression with a cortactin antisense oligo significantly impaired S1P-induced capillary formation, migration of endothelial cells, and actin assembly at the cell periphery. Overexpression of wild-type cortactin tagged by green fluorescent protein (GFP) increased the S1P-induced tube formation and cell motility, whereas the cells overexpressing the mutant formed poorly capillary network and became less motile in response to S1P. Analysis of distribution in Triton X-100 insoluble fractions demonstrated that the cortactin mutant inhibited the association of wild-type cortactin and Arp2/3 complex with the actin-enriched complex. Furthermore, actin polymerization at and distribution of Arp2/3 complex as well as endogenous cortactin into the cell-leading edge mediated by S1P was disturbed. These data suggest that the interaction between cortactin and Arp2/3 complex plays an important role in S1P-mediated remodeling of endothelial cells.
Original language | English (US) |
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Pages (from-to) | 107-121 |
Number of pages | 15 |
Journal | Experimental Cell Research |
Volume | 298 |
Issue number | 1 |
DOIs | |
State | Published - Aug 1 2004 |
Keywords
- Actin cytoskeleton
- Angiogenesis
- Arp2/3 complex
- Cortactin
- EDG
- Endothelial cell
- FACS
- HUVE
- MLCK
- Migration
- S1P
- endothelial differentiation gene
- fluorescence-activated cell sorting
- human umbilical vein endothelial
- myosin light chain kinase
ASJC Scopus subject areas
- Cell Biology