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Neurogenetics. 2011 Feb;12(1):83-6. doi: 10.1007/s10048-010-0261-6. Epub 2010 Sep 23.

Evidence for anti-angiogenic and pro-survival functions of the cerebral cavernous malformation protein 3.

Author information

1
Department of Human Genetics, University of Würzburg, Würzburg, Germany.

Abstract

Mutations in CCM1, CCM2, or CCM3 lead to cerebral cavernous malformations, one of the most common hereditary vascular diseases of the brain. Endothelial cells within these lesions are the main disease compartments. Here, we show that adenoviral CCM3 expression inhibits endothelial cell migration, proliferation, and tube formation while downregulation of endogenous CCM3 results in increased formation of tube-like structures. Adenoviral CCM3 expression does not induce apoptosis under normal endothelial cell culture conditions but protects endothelial cells from staurosporine-induced cell death. Tyrosine kinase activity profiling suggests that CCM3 supports PDPK-1/Akt-mediated endothelial cell quiescence and survival.

PMID:
20862502
PMCID:
PMC3029799
DOI:
10.1007/s10048-010-0261-6
[Indexed for MEDLINE]
Free PMC Article
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