Cilengitide's Effects on Endothelial Cells
Author Information
Author(s): Alghisi Gian Carlo, Ponsonnet Lionel, Rüegg Curzio
Primary Institution: University of Lausanne
Hypothesis
Does cilengitide affect endothelial cells expressing αVβ3 but adhering through β1 integrins?
Conclusion
Cilengitide disrupts VE-cadherin localization and increases permeability in endothelial cells.
Supporting Evidence
- Cilengitide activates αVβ3 and disrupts VE-cadherin localization.
- Cilengitide increases permeability of endothelial cell monolayers.
- Cilengitide induces phosphorylation of Src, FAK, and VE-cadherin.
- Cilengitide interferes with β1 integrin-mediated adhesion.
- Cilengitide causes endothelial cell detachment on low-density ligands.
Takeaway
Cilengitide is a drug that can make blood vessel cells leakier by messing with their connections.
Methodology
The study used morphological, biochemical, pharmacological, and functional approaches to investigate cilengitide's effects on human umbilical vein endothelial cells (HUVEC).
Limitations
The study primarily focuses on in vitro conditions, which may not fully replicate in vivo environments.
Participant Demographics
Human umbilical vein endothelial cells (HUVEC) were used.
Statistical Information
P-Value
p<0.05
Statistical Significance
p<0.05
Digital Object Identifier (DOI)
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