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Cell cycle inhibition provides neuroprotection and reduces glial proliferation and scar formation after traumatic brain injury.
Proc Natl Acad Sci U S A. 2005 Jun 07; 102(23):8333-8.PN

Abstract

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.

Authors+Show Affiliations

Department of Neuroscience, Georgetown University School of Medicine, 3900 Reservoir Road NW, Washington, DC 20057, USA.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

15923260

Citation

Di Giovanni, Simone, et al. "Cell Cycle Inhibition Provides Neuroprotection and Reduces Glial Proliferation and Scar Formation After Traumatic Brain Injury." Proceedings of the National Academy of Sciences of the United States of America, vol. 102, no. 23, 2005, pp. 8333-8.
Di Giovanni S, Movsesyan V, Ahmed F, et al. Cell cycle inhibition provides neuroprotection and reduces glial proliferation and scar formation after traumatic brain injury. Proc Natl Acad Sci USA. 2005;102(23):8333-8.
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 of the United States of America, 102(23), 8333-8.
Di Giovanni S, et al. Cell Cycle Inhibition Provides Neuroprotection and Reduces Glial Proliferation and Scar Formation After Traumatic Brain Injury. Proc Natl Acad Sci USA. 2005 Jun 7;102(23):8333-8. PubMed PMID: 15923260.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Cell cycle inhibition provides neuroprotection and reduces glial proliferation and scar formation after traumatic brain injury. AU - Di Giovanni,Simone, AU - Movsesyan,Vilen, AU - Ahmed,Farid, AU - Cernak,Ibolja, AU - Schinelli,Sergio, AU - Stoica,Bogdan, AU - Faden,Alan I, Y1 - 2005/05/27/ PY - 2005/6/1/pubmed PY - 2005/7/28/medline PY - 2005/6/1/entrez SP - 8333 EP - 8 JF - Proceedings of the National Academy of Sciences of the United States of America JO - Proc. Natl. Acad. Sci. U.S.A. VL - 102 IS - 23 N2 - 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. SN - 0027-8424 UR - https://www.unboundmedicine.com/medline/citation/15923260/Cell_cycle_inhibition_provides_neuroprotection_and_reduces_glial_proliferation_and_scar_formation_after_traumatic_brain_injury_ L2 - http://www.pnas.org/cgi/pmidlookup?view=long&pmid=15923260 DB - PRIME DP - Unbound Medicine ER -