title: Induction of brain arteriovenous malformation in the adult mouse.
abstract: Brain arteriovenous malformations (bAVM) are tangles of abnormal, dilated vessels that directly shunt blood between the arteries and veins. The pathogenesis of bAVM is currently unknown. Patients with hereditary hemorrhagic telangiectasia (HHT) have a higher prevalence of bAVM than the general population. Animal models are important tools for dissecting the disease etiopathogenesis and for testing new therapies. Here, we introduce a method that induces the bAVM phenotype through regional deletion of activin-like kinase 1 (Alk1, the causal gene for HHT2) and vascular endothelial growth factor (VEGF) stimulation.
authors: Department of Anesthesia and Perioperative Care, Center for Cerebrovascular Research, University of California, San Francisco, San Francisco, CA, USA.
authors: Wanqiu
authors: W
authors: Chen
authors: William L
authors: WL
authors: Young
authors: Hua
authors: H
authors: Su
mesh_terms: D030201:Activin Receptors, Type I / Q000235:genetics; D030301:Activin Receptors, Type II; D000818:Animals; D001165:Arteriovenous Malformations / Q000235:genetics* / Q000473:pathology; D002536:Cerebral Arteries / Q000002:abnormalities; D002550:Cerebral Veins / Q000002:abnormalities; D002560:Cerebrovascular Circulation; D004195:Disease Models, Animal; D055786:Gene Knockout Techniques; D051379:Mice; D008822:Mice, Transgenic; D055806:Microvessels / Q000002:abnormalities; D042461:Vascular Endothelial Growth Factor A / Q000502:physiology
chemical_list: D042461:Vascular Endothelial Growth Factor A; C467480:vascular endothelial growth factor A, mouse; D030201:Activin Receptors, Type I; D030301:Activin Receptors, Type II; C498931:Acvrl1 protein, mouse