CoChat
Sign Up
Cited by 164Nerve injury and regenerationNeurogenesis and neuroplasticity mechanismsGlaucoma and retinal disorders

Re-establishing the regenerative potential of central nervous system axons in postnatal mice

Open access
Cho, Kin-Sang, Yang, Liu, Lu, Bin, Feng Ma, Hong, Huang, Xizhong, Pekny, Milos, Chen, Dong Feng·2005·Journal of Cell Science
DOI 10.1242/jcs.01658PMC PMC1351228
Open this paper in CoChat — free account

Abstract

At a certain point in development, axons in the mammalian central nervous system lose their ability to regenerate after injury. Using the optic nerve model, we show that this growth failure coincides with two developmental events: the loss of Bcl-2 expression by neurons and the maturation of astrocytes. Before postnatal day 4, when astrocytes are immature, overexpression of Bcl-2 alone supported robust and rapid optic nerve regeneration over long distances, leading to innervation of brain targets by day 4 in mice. As astrocytes matured after postnatal day 4, axonal regeneration was inhibited in mice overexpressing Bcl-2. Concurrent induction of Bcl-2 and attenuation of reactive gliosis reversed the failure of CNS axonal re-elongation in postnatal mice and led to rapid axonal regeneration over long distances and reinnervation of the brain targets by a majority of severed optic nerve fibers up to 2 weeks of age. These results suggest that an early postnatal downregulation of Bcl-2 and post-traumatic reactive gliosis are two important elements of axon regenerative failure in the CNS.

Integrity signals

Registry

Crossref · 10.1242/jcs.01658

Cites

2 of 2 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Claims the paper makes

We couldn’t retrieve this paper’s full text, so its claims and self-check weren’t run. The registry and citation checks still apply.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • Gfap−/−Vim−/− mice exhibit better posttraumatic regeneration of neuronal synapses and axons, increased baseline and posttraumatic neurogenesis, and improved functional recovery after spinal cord trauma.

    “Interestingly, Gfap−/−Vim−/− mice exhibit better posttraumatic regeneration of neuronal synapses (23) and axons (34), increased baseline and posttraumatic neurogenesis (35), and improved functional recovery after spinal cord trauma (36).”

    From Attenuating astrocyte activation accelerates plaque pathogenesis in APP/PS1 mice (2013) · cites this paper as [34]

Cites

Flagged first, then by citations

Cited by

Sorted by citations

Authors
Cho, K.-S., Yang, L., Lu, B., Feng Ma, H., Huang, X., Pekny, M., & Chen, D. F.
Affiliations
  • Harvard University (US)
  • Schepens Eye Research Institute, Program in Neuroscience and Department of Ophthalmology, Harvard Medical School, 20 Staniford Street, Boston, MA 02114, USA
  • University of Gothenburg (SE)
ORCID
Venue
Journal of Cell Science
Publisher
The Company of Biologists
Published
2005-03-01
Volume
118
Issue
5
Pages
863-872
ISSN
  • 0021-9533 (ISSN-L)
  • 1477-9137
DOI
10.1242/jcs.01658
PMC
PMC1351228
OpenAlex
W2059143929
Cited by
164
References
2
Citations by year
2026: 4 · 2025: 6 · 2024: 2 · 2023: 2 · 2022: 3 · 2021: 5 · 2020: 5 · 2019: 6 · 2018: 9 · 2017: 4 · 2016: 6 · 2015: 14 · 2014: 8 · 2013: 10 · 2012: 15
FWCI
4.47
Type
journal article
Language
en
Open access
Locations
  • Journal of Cell Science (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
  • HighWire Press Open Archive (submittedVersion)
Funders
National Eye Institute (R01EY012983)
Topics
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nerve injury and regeneration
  • Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
  • Health Sciences › Medicine › Ophthalmology › Glaucoma and retinal disorders
Keywords
axon regeneration, central nervous system, optic nerve, Bcl-2, astrocyte maturation, reactive gliosis, postnatal development, reinnervation, neuronal survival, axon growth inhibition
MeSH terms
Animals, Animals, Newborn, Astrocytes, Axons, Brain, Central Nervous System, Female, Glial Fibrillary Acidic Protein, Gliosis, Humans, Male, Mice, Inbred C57BL, Mice, Transgenic, Microscopy, Fluorescence, Models, Anatomic, Nerve Regeneration, Neurons, Optic Nerve, Retina, Vimentin, Blotting, Western, Down-Regulation, DNA Primers, Coculture Techniques, Transgenes, Proto-Oncogene Proteins c-bcl-2, Reverse Transcriptase Polymerase Chain Reaction, Microscopy, Electron, Transmission, Mice

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review