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Centrosome reorientation in regenerating endothelial monolayers requires bFGF
1Department of Biomedical Sciences, Ontario Veterinary College, University of Guelph, Ontario, Canada.
Journal of Cellular Biochemistry
|July 1, 1993
Summary
Basic fibroblast growth factor (bFGF) is crucial for endothelial cell monolayer regeneration after injury. Inhibiting bFGF blocks cell repair, lamellipodia formation, and centrosome reorientation, highlighting bFGF
Area of Science:
- Cell Biology
- Wound Healing
- Endothelial Cell Function
Background:
- Endothelial cells repair denudation via lamellipodia, migration, and proliferation.
- Basic fibroblast growth factor (bFGF) is essential for this regeneration process.
- Centrosome reorientation is proposed to be key for cell polarization and migration.
Purpose of the Study:
- To investigate the effects of anti-bFGF antibodies and suramin on endothelial monolayer regeneration.
- To assess the impact on actin microfilament staining and centrosome orientation.
- To determine the role of bFGF in cell spreading and centrosome reorientation during repair.
Main Methods:
- Cultured bovine large vessel endothelial cells were partially denuded.
- Treatments included polyclonal antibody to bFGF and suramin.
- Assessed monolayer regeneration, actin staining, and centrosome orientation at the wound edge.
Main Results:
- Anti-bFGF and suramin treatments abolished monolayer repair.
- Cells showed altered actin patterns, reduced lamellipodia extrusion, and inhibited centrosome reorientation.
- Exogenous bFGF restored repair and reorientation in antibody-treated cells, but not suramin-treated cells.
Conclusions:
- bFGF availability is critical for endothelial monolayer regeneration.
- Interference with bFGF impacts cell spreading and centrosome reorientation.
- These mechanisms are vital for endothelial wound healing.