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Article type: Research Article
Authors: Jahroudi, Nadiaa; * | Schmaier, Alvinb | Srikanth, Sujatab | Mahdi, Fakhrib | Lutka, Frances A.c | Bowser, Robertc
Affiliations: [a] Department of Medicine, Division of Cardiology, Albert Einstein College of Medicine, Bronx, NY, USA | [b] Division of Hematology and Oncology, Departments of Internal Medicine and Pathology, University of Michigan, Ann Arbor, MI, USA | [c] Department of Pathology, Division of Neuropathology, University of Pittsburgh, Pittsburgh, PA, USA
Correspondence: [*] Corresponding author: Nadia Jahroudi, F717, Forchheimer Building, Department of Medicine, Division of Cardiology, Albert Einstein College of Medicine, 1300 Morris Park Ave, Bronx, NY 10461, USA. Tel.: +1 718 430 3295; Fax: +1 718 430 8989; E-mail: [email protected].
Abstract: Dysfunction of brain vascular endothelial cells may be associated with the pathogenesis of several diseases including cerebral amyloid angiopathy, hemorrhagic stroke and Alzheimer disease. New model systems are necessary to examine the contribution of brain endothelial cells in these disorders. The Von Willebrand factor gene promoter fragment that spans sequences -487 to +247 targets the expression of LacZ marker gene in transgenic mice specifically to brain vascular endothelial cells. Transgenic mice have been prepared that express human amyloid β protein precursor protein (AβPP) isoforms 695 and 751 (wild-type and Dutch variant mutations) under the regulation of this VWF promoter sequence. These AβPP transgenes are specifically expressed in brain vascular endothelial cells. The VWF promoter is a valuable tool for targeting gene expression to brain vascular endothelial cells to provide a model to directly examine endothelial cell placement of genes and their contribution to cerebral vascular disease.
Keywords: amyloid β-protein precursor, von Willebrand factor promoter, transgenic mice, cerebral amyloid angiopathy, endothelial cells
DOI: 10.3233/JAD-2003-5209
Journal: Journal of Alzheimer's Disease, vol. 5, no. 2, pp. 149-158, 2003
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