Minimal Homozygous Endothelial Deletion of Eng with VEGF Stimulation Is Sufficient to Cause Cerebrovascular Dysplasia in the Adult Mouse | Zendy

EunJung Choi | Zendy; Espen J. Walker | Zendy; Fanxia Shen | Zendy; S. Paul Oh | Zendy; Helen M. Arthur | Zendy; William L. Young | Zendy; Hua Su | Zendy

Open Access

Minimal Homozygous Endothelial Deletion of Eng with VEGF Stimulation Is Sufficient to Cause Cerebrovascular Dysplasia in the Adult Mouse

Author(s) -

EunJung Choi,

Espen J. Walker,

Fanxia Shen,

S. Paul Oh,

Helen M. Arthur,

William L. Young,

Hua Su

Publication year - 2012

Publication title -

cerebrovascular diseases

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.221

H-Index - 104

eISSN - 1421-9786

pISSN - 1015-9770

DOI - 10.1159/000337762

Subject(s) - medicine , endoglin , dysplasia , vascular endothelial growth factor , pathology , viral vector , telangiectasia , angiogenesis , exon , vegf receptors , biology , gene , cd34 , genetics , stem cell , recombinant dna

Brain arteriovenous malformations (bAVMs) represent a high risk for hemorrhagic stroke, leading to significant neurological morbidity and mortality in young adults. The etiopathogenesis of bAVM remains unclear. Research progress has been hampered by the lack of animal models. Hereditary Hemorrhagic Telangiectasia (HHT) patients with haploinsufficiency of endoglin (ENG, HHT1) or activin receptor-like kinase 1 (ALK1, HHT2) have a higher incidence of bAVM than the general population. We previously induced cerebrovascular dysplasia in the adult mouse that resembles human bAVM through Alk1 deletion plus vascular endothelial growth factor (VEGF) stimulation. We hypothesized that Eng deletion plus VEGF stimulation would induce a similar degree of cerebrovascular dysplasia as the Alk1-deleted brain.

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