Related Experiment Videos
TEM8 expression stimulates endothelial cell adhesion and migration by regulating cell-matrix interactions on collagen
Kylie A Hotchkiss1, Cheryl M Basile, Simone C Spring
1Department of Medicine, Albert Einstein College of Medicine, Bronx, New York 10461, USA.
Experimental Cell Research
|March 22, 2005
Summary
Tumor blood vessel protein TEM8 (TROY) enhances endothelial cell migration and adhesion to collagen, promoting angiogenesis. Blocking TEM8 function inhibits these pro-angiogenic activities.
Area of Science:
- Molecular Biology
- Cell Biology
- Angiogenesis Research
Background:
- The TEM8 gene is specifically found in tumor blood vessels, but its role in endothelial cell function remains unclear.
- Understanding TEM8's function is crucial for developing targeted cancer therapies that disrupt tumor vasculature.
Purpose of the Study:
- To investigate the function of TEM8 in endothelial cell biology.
- To determine how TEM8 overexpression or inhibition affects endothelial cell activities, particularly migration and adhesion.
Main Methods:
- Assessed endothelial cell migration using monolayer denudation and Boyden chamber assays.
- Utilized recombinant TEM8 extracellular domain (TEM8-ED) to inhibit TEM8 function.
- Measured endothelial cell adhesion to collagen and beta1 integrin activation.
Main Results:
- TEM8 overexpression significantly increased endothelial cell migration (3-fold).
- TEM8-ED inhibited both chemokinetic and chemotactic migration on collagen.
- TEM8 enhanced endothelial cell adhesion to collagen, an effect reversed by TEM8-ED; TEM8-ED did not affect beta1 integrin activation.
- TEM8 expression increased 5-fold during in vitro tube formation, correlating with angiogenesis.
Conclusions:
- TEM8 plays a positive role in endothelial cell migration and adhesion, processes critical for angiogenesis.
- TEM8 is a key regulator of endothelial cell behavior in the context of blood vessel formation.