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Cited by 421Nerve injury and regenerationNeurogenesis and neuroplasticity mechanismsAxon Guidance and Neuronal Signaling

The DOI matches its Crossref record; 90 of the 90 references it cites were found in a registry or an index.

Growth-associated gene expression after stroke: evidence for a growth-promoting region in peri-infarct cortex

Carmichael, S. Thomas, Archibeque, Ivonne, Luke, Linslee, Nolan, Tim, Momiy, Janneth, Li, Songlin·2005·Experimental Neurology
DOI 10.1016/j.expneurol.2005.01.004
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Abstract

Stroke induces axonal sprouting in peri-infarct cortex. A set of growth-associated genes important in axonal sprouting in peripheral nervous system regeneration and cortical development has recently been defined. The expression profiles of these growth-associated genes were defined during the post-stroke axonal sprouting response using a model of stroke in barrel field cortex. Stroke induces sequential waves of neuronal growth-promoting genes during the sprouting response: an early expression peak (SPRR1), a mid expression peak (p21, Ta1 tubulin, L1, MARCKS), a late peak (SCG10, SCLIP), and an early/sustained pattern (GAP43, CAP23, c-jun). These expression peaks correspond to specific time points in the sprouting response. The expression of the growth-inhibiting chondroitin sulfate proteoglycans aggrecan, brevican, versican, and phosphacan are induced late in the sprouting process; except neurocan, which is increased during the peak of the growth-promoting gene expression. The developmentally associated growth inhibitors ephrin-A5, ephB1, semaphorin IIIa, and neuropilin 1 are also induced in the early phases of the sprouting response. At the cellular level, chondroitin sulfate proteoglycans, in the form of peri-neuronal nets, are reduced in the region of axonal sprouting, during the peak of growth-promoting gene expression. These results identify a unique profile of growth-promoting gene expression in adult cortex after stroke, the inhibitory molecules that are present during the sprouting response, and a region in which growth-promoting genes are increased, growth-inhibitory proteins are diminished and axonal sprouting occurs. This region may be a growth-promoting zone after stroke.

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Crossref · 10.1016/j.expneurol.2005.01.004

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Research works printed but not linked: 1

  1. Li, S., Zheng, J., Carmichel, S.T., in press. Differences in ischemic injury after stroke between aged and young adults. Neurobiol. Dis.

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Metadata

Authors
Carmichael, S. T., Archibeque, I., Luke, L., Nolan, T., Momiy, J., & Li, S.
Affiliations
University of California, Los Angeles (US)
Corresponding author
Carmichael, S. Thomas
ORCID
Venue
Experimental Neurology
Publisher
Elsevier BV
Published
2005-06
Volume
193
Issue
2
Pages
291-311
ISSN
0014-4886 (ISSN-L)
DOI
10.1016/j.expneurol.2005.01.004
OpenAlex
W1997912239
Cited by
421
References
89
Citations by year
2026: 10 · 2025: 13 · 2024: 14 · 2023: 12 · 2022: 18 · 2021: 15 · 2020: 21 · 2019: 21 · 2018: 23 · 2017: 24 · 2016: 29 · 2015: 20 · 2014: 26 · 2013: 35 · 2012: 25
FWCI
5.52
Type
journal article
Language
en
Open access
closed
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations
  • Experimental Neurology (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health
  • National Institute of Neurological Disorders and Stroke (R01NS045729)
Topics
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nerve injury and regeneration
  • Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Axon Guidance and Neuronal Signaling
Keywords
stroke, axonal sprouting, peri-infarct cortex, chondroitin sulfate proteoglycans, growth inhibitors, ephrin-A5, neuropilin-1, EphB1, GAP-43, c-Jun, neuroplasticity
MeSH terms
Animals, Cerebral Cortex, Chondroitin Sulfates, Disease Models, Animal, Gene Expression Regulation, Immunohistochemistry, Male, Nerve Growth Factors, Nerve Tissue Proteins, Chondroitin Sulfate Proteoglycans, Proteoglycans, Rats, Inbred F344, RNA, Messenger, Time Factors, Gene Expression, Extracellular Matrix Proteins, In Situ Hybridization, Reverse Transcriptase Polymerase Chain Reaction, Brain Infarction, Stroke, Lectins, C-Type, Rats, Aggrecans, Versicans, Receptor-Like Protein Tyrosine Phosphatases, Class 5

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