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MAIN Science News: Paper published on "A novel protein on cells of the blood vessel w

 
 
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MAIN Science News: Paper published on "A novel protein on cells of the blood vessel w
Dietmar Vestweber,  at the University of Muenster and LIC in MAIN has had an article on
"A novel protein on cells of the blood vessel wall involved in the regulation of the opening of cell contacts"
published in the prestigious Journal of Experimental Medicine, July 2006.

Vestweber & his teams' overall scientific goals include: understanding how leukocytes overcome the barrier of the blood vessel wall & how various known and unknown cell adhesion mechanisms mediate and control the opening and closure of endothelial cell contacts and the movement of leukocytes through the contact sites between endothelial cells.
A brief abstract of the article has been provided as follows:

We have recently identified a new molecule, endothelial cell-selective adhesion molecule (ESAM) that is specifically located at cell contacts between endothelial cells. These cells form the inner layer of the blood vessel wall and control the exit of cells and molecules from the blood into the surrounding tissue. This is the central function that controls vascular permeability as well as the entry of leukocytes into inflamed tissue, the step that initiates the process of inflammation. In a recent paper published in the Journal of Experimental Medicine (http://www.jem.org/cgi/content/full/203/7/1671; July 2006, 203(7) pp. 1671-1677) we showed that ESAM is involved in the opening of endothelial cell contacts as well as in the control of leukocyte extravasation. Transgenic mice were generated with a disruption in the corresponding gene leading to the loss of ESAM at endothelial cell contacts. These mice recruited leukocytes more slowly into inflamed tissue than wild type mice. In addition, stimuli that induce increased permeability of the vessel wall, such as the vascular endothelial growth factor (VEGF), increased permeability less dramatically in the transgenic mice. These results establish ESAM as a novel player in the control of endothelial cell contact in blood vessels.