Plasmalemmal Vesicle Associated Protein-1 (PV-1) is a marker of blood-brain barrier disruption in rodent models

<p>Abstract</p> <p>Background</p> <p><it>Plasmalemmal vesicle associated protein-1 </it>(<it>PV-1</it>) is selectively expressed in human brain microvascular endothelial cells derived from clinical specimens of primary and secondary malignant bra...

Full description

Bibliographic Details
Main Authors: Ali Zarina S, Winans Bethany N, Liu Yang, Carson-Walter Eleanor B, Shue Eveline H, Chen Jun, Walter Kevin A
Format: Article
Language:English
Published: BMC 2008-02-01
Series:BMC Neuroscience
Online Access:http://www.biomedcentral.com/1471-2202/9/29
Description
Summary:<p>Abstract</p> <p>Background</p> <p><it>Plasmalemmal vesicle associated protein-1 </it>(<it>PV-1</it>) is selectively expressed in human brain microvascular endothelial cells derived from clinical specimens of primary and secondary malignant brain tumors, cerebral ischemia, and other central nervous system (CNS) diseases associated with blood-brain barrier breakdown. In this study, we characterize the murine CNS expression pattern of <it>PV-1 </it>to determine whether localized <it>PV-1 </it>induction is conserved across species and disease state.</p> <p>Results</p> <p>We demonstrate that <it>PV-1 </it>is selectively upregulated in mouse blood vessels recruited by brain tumor xenografts at the RNA and protein levels, but is not detected in non-neoplastic brain. Additionally, <it>PV-1 </it>is induced in a mouse model of acute ischemia. Expression is confined to the cerebovasculature within the region of infarct and is temporally regulated.</p> <p>Conclusion</p> <p>Our results confirm that <it>PV-1 </it>is preferentially induced in the endothelium of mouse brain tumors and acute ischemic brain tissue and corresponds to blood-brain barrier disruption in a fashion analogous to human patients. Characterization of <it>PV-1 </it>expression in mouse brain is the first step towards development of rodent models for testing anti-edema and anti-angiogenesis therapeutic strategies based on this molecule.</p>
ISSN:1471-2202