Plasmalemmal vesicle associated protein-1 (PV-1) is a marker of blood-brain barrier disruption in rodent models
EH Shue, EB Carson-Walter, Y Liu, BN Winans… - BMC neuroscience, 2008 - Springer
EH Shue, EB Carson-Walter, Y Liu, BN Winans, ZS Ali, J Chen, KA Walter
BMC neuroscience, 2008•SpringerBackground Plasmalemmal vesicle associated protein-1 (PV-1) 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 PV-1 to determine whether localized PV-
1 induction is conserved across species and disease state. Results We demonstrate that PV …
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 PV-1 to determine whether localized PV-
1 induction is conserved across species and disease state. Results We demonstrate that PV …
Background
Plasmalemmal vesicle associated protein-1 (PV-1) 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 PV-1 to determine whether localized PV-1 induction is conserved across species and disease state.
Results
We demonstrate that PV-1 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, PV-1 is induced in a mouse model of acute ischemia. Expression is confined to the cerebovasculature within the region of infarct and is temporally regulated.
Conclusion
Our results confirm that PV-1 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 PV-1 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.
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