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De Novo Cerebrovascular Malformation in the Adult Mouse After Endothelial Alk1 Deletion and Angiogenic Stimulation
Author(s) -
Wanqiu Chen,
Zhengda Sun,
Zhenying Han,
Kristine Jun,
Marine Camus,
Mamta Wankhede,
Lei Mao,
Tom Arnold,
William L. Young,
Hua Su
Publication year - 2014
Publication title -
stroke
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.397
H-Index - 319
eISSN - 1524-4628
pISSN - 0039-2499
DOI - 10.1161/strokeaha.113.003655
Subject(s) - pdgfb , angiogenesis , medicine , vascular endothelial growth factor , tamoxifen , pathology , stimulation , proliferation index , growth factor , cortical dysplasia , endocrinology , receptor , epilepsy , immunohistochemistry , platelet derived growth factor receptor , vegf receptors , cancer , breast cancer , psychiatry
In humans, activin receptor-like kinase 1 (Alk1) deficiency causes arteriovenous malformations (AVMs) in multiple organs, including the brain. Focal Alk1 pan-cellular deletion plus vascular endothelial growth factor stimulation induces brain AVMs in the adult mouse. We hypothesized that deletion of Alk1 in endothelial cell (EC) alone plus focal vascular endothelial growth factor stimulation is sufficient to induce brain AVM in the adult mouse.

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