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Up-Regulation of Neuropilin-1 in Neovasculature after Focal Cerebral Ischemia in the Adult Rat
Abstract
During development, neuropilin-1 is a receptor for semaphorin 3a-mediated axonal guidance and for vascular endothelial growth factor (VEGF) promotion of angiogenesis. The authors measured neuropilin-1 expression in the adult ischemic brain using Northern blot, in situ hybridization, and immunohistochemistry. Neuropilin-1 mRNA was significantly up-regulated as early as 2 hours and persisted at least 28 days after focal cerebral ischemia. Acute up-regulation of neuropilin-1 mRNA primarily localized to the ischemic neurons. A marked increase in both mRNA and protein of neuropilin-1 was detected in endothelial cells of cerebral blood vessels at the border and in the core of the ischemic lesion 7 days after ischemia, and neuropilin-1 gene expression persisted on these vessels for at least 28 days after ischemia. In these areas, neovascularization was detected using three-dimensional reconstructed images obtained from laser scanning confocal microscopy. Activated astrocytes also exhibited neuropilin-1 immunoreactivity during 7 to 28 days of ischemia. Double immunofluorescent staining showed colocalization of neuropilin-1 and VEGF to cerebral blood vessels and activated astrocytes. These data suggest that in addition to its role in axonal growth, up-regulation of neuropilin-1, in concert with VEGF and its receptors, may contribute to neovascular formation in the adult ischemic brain.
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Neuropilin is required for guidance of tip cells during sprouting angiogenesis, by balancing pro-angiogenic and anti-angiogenic signals between major pathways including VEGF, semaphorins and Wnt signaling; its upregulation in vessels contributes to BBB breakdown during brain injury and inflammation.
“Neuropilin, a common co-receptor and regulator of many morphogens and growth factors, is required for guidance of tip cells during spouting angiogenesis (127), by balancing the pro-angiogenic and anti-angiogenic signals between major pathways including VEGF, semaphorins and Wnt signaling; its upregulation in vessels contributes to BBB breakdown during brain injury and inflammation (564, 679).”
From Blood-Brain Barrier: From Physiology to Disease and Back (2019) · cites this paper as [679]
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Metadata
- Authors
- Zhang, Z. G., Tsang, W., Zhang, L., Powers, C., & Chopp, M.
- Affiliations
- Henry Ford Health (US)
- Venue
- Journal of Cerebral Blood Flow & Metabolism
- Publisher
- SAGE Publications
- Published
- 2001-05
- Volume
- 21
- Issue
- 5
- Pages
- 541-549
- ISSN
- 0271-678X (ISSN-L)
- 1559-7016
- OpenAlex
- W2021842070
- Cited by
- 84
- References
- 36
- Citations by year
- 2024: 2 · 2023: 1 · 2022: 3 · 2021: 2 · 2020: 1 · 2019: 1 · 2018: 1 · 2017: 1 · 2016: 2 · 2015: 5 · 2014: 3 · 2013: 4 · 2012: 5
- FWCI
- 2.33
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Cerebral Blood Flow & Metabolism (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (5r01ns033627-08)
- National Institute of Neurological Disorders and Stroke (P01NS23393, R01NS-33627, P01NS023393)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Angiogenesis and VEGF in Cancer
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Axon Guidance and Neuronal Signaling
- Life Sciences › Neuroscience › Neurology › Barrier Structure and Function Studies
- Keywords
- neuropilin-1, focal cerebral ischemia, neovascularization, vascular endothelial growth factor, angiogenesis, ischemic neurons, endothelial cells, semaphorin 3A, axon guidance, ischemic brain
- MeSH terms
- Animals, Astrocytes, Brain, Capillaries, Brain Ischemia, Endothelium, Vascular, Lymphokines, Male, Nerve Tissue Proteins, RNA, Messenger, Blotting, Northern, Up-Regulation, Endothelial Growth Factors, Rats, Wistar, In Situ Hybridization, DNA, Complementary, Microscopy, Confocal, Neovascularization, Physiologic, Neuropilin-1, Vascular Endothelial Growth Factors, Vascular Endothelial Growth Factor A, Rats
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