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Sci. Signal., 10 March 2009
Vol. 2, Issue 61, p. ra10
[DOI: 10.1126/scisignal.2000162]


Editor's Summary

Bypassing the Barrier
In ischemic stroke and various neurological disorders, neuronal death is exacerbated by breakdown of the blood-brain barrier, composed of vascular endothelial cells, the underlying basal lamina, and associated glial cells. Noting that the small guanosine triphosphatase Rac1 has been implicated in various aspects of endothelial cell function, Sawada et al. used transgenic mice to explore the contribution of endothelial Rac1 to neuronal damage and the breakdown of vascular integrity in a mouse model of ischemic stroke. Mice with decreased endothelial Rac1 abundance showed a reduction in infarct size, brain edema, and neurological deficits. Endothelial cells from these mice showed increased expression of genes implicated in the stress response, as well as genes encoding neurotrophic factors and components of the basement membrane. Intriguingly, Rac-deficient brain endothelial cells showed enhanced production of the neurotrophic factor artemin. Thus, endothelial Rac1 may represent a viable therapeutic target in ischemic stroke and other conditions associated with neuronal death and breakdown of blood-brain barrier function.

Citation: N. Sawada, H.-H. Kim, M. A. Moskowitz, J. K. Liao, Rac1 Is a Critical Mediator of Endothelium-Derived Neurotrophic Activity. Sci. Signal. 2, ra10 (2009).

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