The DOI matches its Crossref record; 42 of the 42 references it cites were found in a registry or an index.
Cell cycle inhibition provides neuroprotection and reduces glial proliferation and scar formation after traumatic brain injury
Open accessAbstract
Traumatic brain injury (TBI) causes neuronal apoptosis, inflammation, and reactive astrogliosis, which contribute to secondary tissue loss, impaired regeneration, and associated functional disabilities. Here, we show that up-regulation of cell cycle components is associated with caspase-mediated neuronal apoptosis and glial proliferation after TBI in rats. In primary neuronal and astrocyte cultures, cell cycle inhibition (including the cyclin-dependent kinase inhibitors flavopiridol, roscovitine, and olomoucine) reduced up-regulation of cell cycle proteins, limited neuronal cell death after etoposide-induced DNA damage, and attenuated astrocyte proliferation. After TBI in rats, flavopiridol reduced cyclin D1 expression in neurons and glia in ipsilateral cortex and hippocampus. Treatment also decreased neuronal cell death and lesion volume, reduced astroglial scar formation and microglial activation, and improved motor and cognitive recovery. The ability of cell cycle inhibition to decrease both neuronal cell death and reactive gliosis after experimental TBI suggests that this treatment approach may be useful clinically.
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Cites
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Cyclin D1 is an essential mediator of apoptotic neuronal cell death.
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Cell Cycle Activation Linked to Neuronal Cell Death Initiated by DNA Damage
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Cited by
Blood–brain barrier breakdown as a therapeutic target in traumatic brain injury
Shlosberg, D., Benifla, M., Kaufer, D., & Friedman, A. (2010) · Nature Reviews Neurology · doi:10.1038/nrneurol.2010.74 · Cited by 897
Neuroinflammation after traumatic brain injury: Opportunities for therapeutic intervention
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Self-citationPathophysiology of traumatic brain injury
Greve, M. W., & Zink, B. J. (2009) · Mount Sinai Journal of Medicine: A Journal of Translational and Personalized Medicine · doi:10.1002/msj.20104 · Cited by 477
Long-lasting arrest of murine polycystic kidney disease with CDK inhibitor roscovitine
Bukanov, N. O., Smith, L. A., Klinger, K. W., Ledbetter, S. R., & Ibraghimov-Beskrovnaya, O. (2006) · Nature · doi:10.1038/nature05348 · Cited by 276
Metadata
- Authors
- Di Giovanni, S., Movsesyan, V., Ahmed, F., Cernak, I., Schinelli, S., Stoica, B., & Faden, A. I.
- Venue
- Proceedings of the National Academy of Sciences
- Published
- 2005-05-27
- Volume
- 102
- Issue
- 23
- Pages
- 8333-8338
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- OpenAlex
- W2145278696
- Cited by
- 377
- References
- 42
- FWCI
- 12.10
- Type
- journal article
- Language
- en
- Open access
- green
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- Di Giovanni, S., Movsesyan, V., Ahmed, F., Cernak, I., Schinelli, S., Stoica, B., & Faden, A. I. (2005). Cell cycle inhibition provides neuroprotection and reduces glial proliferation and scar formation after traumatic brain injury. Proceedings of the National Academy of Sciences. https://doi.org/10.1073/pnas.0500989102
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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