Down‐regulation of neurocan expression in reactive astrocytes promotes axonal regeneration and facilitates the neurorestorative effects of bone marrow stromal cells in the ischemic rat brain
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The glial scar, a primarily astrocytic structure bordering the infarct tissue inhibits axonal regeneration after stroke. Neurocan, an axonal extension inhibitory molecule, is up‐regulated in the scar region after stroke. Bone marrow stromal cells (BMSCs) reduce the thickness of glial scar wall and facilitate axonal remodeling in the ischemic boundary zone. To further clarify the role of BMSCs in axonal regeneration and its underlying mechanism, the current study focused on the effect of BMSCs on neurocan expression in the ischemic brain. Thirty‐one adult male Wistar rats were subjected to 2 h of middle cerebral artery occlusion followed by an injection of 3 × 10 6 rat BMSCs (n = 16) or phosphate‐buffered saline (n = 15) into the tail vein 24 h later. Animals were sacrificed at 8 days after stroke. Immunostaining analysis showed that reactive astrocytes were the primary source of neurocan, and BMSC‐treated animals had significantly lower neurocan and higher growth associated protein 43 expression in the penumbral region compared with control rats, which was confirmed by Western blot analysis of the brain tissue. To further investigate the effects of BMSCs on astrocyte neurocan expression, single reactive astrocytes were collected from the ischemic boundary zone using laser capture microdissection. Neurocan gene expression was significantly down‐regulated in rats receiving BMSC transplantation (n = 4/group). Primary cultured astrocytes showed similar alterations; BMSC coculture during reoxygenation abolished the up‐regulation of neurocan gene in astrocytes undergoing oxygen‐glucose deprivation (n = 3/group). Our data suggest that BMSCs promote axonal regeneration by reducing neurocan expression in peri‐infarct astrocytes. © 2008 Wiley‐Liss, Inc.
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Therapeutic interventions promoting axonal plasticity, such as VEGF or bone-marrow-derived stromal cells, further decrease proteoglycan levels.
“Therapeutic inter ventions promoting axonal plasticity, such as delivery of VEGF or bone-marrow-derived stromal cells, further decrease proteoglycan levels.24,65”
From Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation (2012) · cites this paper as [65]
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- Authors
- Shen, L. H., Li, Y., Gao, Q., Savant‐Bhonsale, S., & Chopp, M.
- Affiliations
- Henry Ford Health (US)
- Corresponding author
- Chopp, Michael
- Venue
- Glia
- Publisher
- Wiley
- Published
- 2008-07-10
- Volume
- 56
- Issue
- 16
- Pages
- 1747-1754
- ISSN
- 0894-1491 (ISSN-L)
- 1098-1136
- PMC
- PMC2575136
- OpenAlex
- W2116308146
- Cited by
- 122
- References
- 51
- Citations by year
- 2026: 1 · 2025: 5 · 2024: 2 · 2023: 11 · 2022: 6 · 2021: 9 · 2020: 4 · 2019: 6 · 2018: 4 · 2017: 5 · 2016: 11 · 2015: 10 · 2014: 11 · 2013: 10 · 2012: 11
- FWCI
- 2.31
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Glia (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute of Neurological Disorders and Stroke (R01NS045041, P01NS42345, P01NS042345, R01 NS45041)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nerve injury and regeneration
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Genetics › Mesenchymal stem cell research
- Keywords
- neurocan, reactive astrocytes, mesenchymal stem cells, axon regeneration, stroke, ischemic brain, glial scar, growth-associated protein 43, cell transplantation, peri-infarct zone, oxygen-glucose deprivation, neurorestoration
- MeSH terms
- Animals, Astrocytes, Cells, Cultured, Gliosis, Male, Nerve Regeneration, Nerve Tissue Proteins, Chondroitin Sulfate Proteoglycans, Proteoglycans, Down-Regulation, Bone Marrow Transplantation, Stromal Cells, Rats, Wistar, GAP-43 Protein, Recovery of Function, Infarction, Middle Cerebral Artery, Growth Cones, Brain Infarction, Hypoxia-Ischemia, Brain, Rats, Neurocan
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