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Blood‐spinal cord barrier after spinal cord injury: Relation to revascularization and wound healing
Open accessAbstract
Spinal cord injury produces prominent disruption of the blood‐spinal cord barrier. We have defined the blood‐spinal cord barrier breakdown to the protein luciferase (61 kDa) in the acutely injured murine spinal cord and during revascularization. We show that newly formed and regenerating blood vessels that have abnormal permeability exhibit differential expression of the glucose‐1 transporter (Glut‐1), and that its expression is dependent on astrocytes. There was overt extravasation of luciferase within the first hour after injury, a period that coincided with marked tissue disruption within the epicenter of the lesion. Although there was a significant reduction in the number of blood vessels relative to controls by 24 hr after injury, abnormal barrier permeability remained significantly elevated. A second peak of abnormal barrier permeability at 3–7 days postinjury coincided with prominent revascularization of the epicenter. The barrier to luciferase was restored by 21 days postinjury and vascularity was similar to that of controls. During wound‐healing process, the cord was reorganized into distinct domains. Between 14 and 21 days postinjury, each domain consisted primarily of nonneuronal cells, including macrophages. Astrocytes were limited characteristically to the perimeter of each domain. Only blood vessels affiliated closely with astrocytes in the perimeter expressed Glut‐1, whereas blood vessels within each domain of the repairing cord did not express it. Together, these data demonstrate that both injured and regenerating vessels exhibit abnormal permeability and suggest that Glut‐1 expression during revascularization is dependent on the presence of astrocytes. © 2003 Wiley‐Liss, Inc.
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“Some reports suggest that SCI generates a biphasic opening of the barrier. The first peak of abnormal leakage occurs within several hours after injury, whereas the second peak is evident between 3 and 7 days post-injury (644).”
From Blood-Brain Barrier: From Physiology to Disease and Back (2019) · cites this paper as [644]
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Metadata
- Authors
- Whetstone, W. D., Hsu, J. C., Eisenberg, M., Werb, Z., & Noble‐Haeusslein, L. J.
- Affiliations
- University of California, San Francisco (US)
- Corresponding author
- Noble‐Haeusslein, Linda J.
- Venue
- Journal of Neuroscience Research
- Publisher
- Wiley
- Published
- 2003-08-25
- Volume
- 74
- Issue
- 2
- Pages
- 227-239
- ISSN
- 0360-4012 (ISSN-L)
- 1097-4547
- PMC
- PMC2837839
- OpenAlex
- W2141244009
- Cited by
- 288
- References
- 42
- Citations by year
- 2026: 14 · 2025: 11 · 2024: 19 · 2023: 23 · 2022: 19 · 2021: 16 · 2020: 17 · 2019: 10 · 2018: 19 · 2017: 9 · 2016: 18 · 2015: 11 · 2014: 13 · 2013: 11 · 2012: 7
- FWCI
- 2.85
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Journal of Neuroscience Research (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute of Neurological Disorders and Stroke (NS 39847, NS39278, R01NS039847, R01NS039278)
- Topics
- Health Sciences › Medicine › Clinical Neurology › Spinal Cord Injury Research
- Life Sciences › Neuroscience › Neurology › Barrier Structure and Function Studies
- Health Sciences › Medicine › Clinical Neurology › Traumatic Brain Injury and Neurovascular Disturbances
- Keywords
- blood-spinal cord barrier, spinal cord injury, revascularization, wound healing, vascular permeability, glucose transporter 1, astrocytes, macrophages, vascular regeneration
- MeSH terms
- Animals, Astrocytes, Blood Vessels, Blood-Brain Barrier, Gliosis, Luciferases, Macrophages, Male, Mice, Inbred C57BL, Spinal Cord, Spinal Cord Injuries, Wound Healing, Glutamic Acid, Neovascularization, Physiologic, Excitatory Amino Acid Transporter 2, Mice
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