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MeSH Review

Trauma, Nervous System

 
 
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High impact information on Trauma, Nervous System

  • The discovery and elaboration of the neuronal apoptotic E2F pathway provides abundant targets as well as small molecule candidates for potential therapeutic intervention in nervous system trauma and degenerative disease [1].
  • A few groups have now shown that overproduction of HSP70 leads to protection in several different models of nervous system injury [2].
  • In this context, the protein kinase C (PKC) family of enzymes are important signalling molecules that play a role in preventing neurodegeneration after nervous system injury [3].
  • Unexpectedly, GH and SOCS2 have been recently shown to regulate neural development, neural stem cell differentiation and neuronal growth -- functions that might have important therapeutic implications for both repairing nervous system injuries and treating neurological disease [4].
  • These data suggest that chronic neuropathic pain is sensitive to early spinal BDNF levels after partial nerve injury and that rAAV-mediated gene transfer could potentially be used to reverse chronic pain after nervous system injuries in humans [5].
 

Chemical compound and disease context of Trauma, Nervous System

 

Anatomical context of Trauma, Nervous System

 

Gene context of Trauma, Nervous System

  • This robust in vitro and in vivo SB 239063-induced neuroprotection emphasizes the potential role of MAPK pathways in ischemic stroke and also suggests that p38 inhibition warrants further study, including protection in other models of nervous system injury and neurodegeneration [13].
  • In response to many stresses and pathologic states, including different models of nervous system injury, cells synthesize a variety of proteins, most notably the inducible 72 kDa heat shock protein 70 (Hsp70), which plays important roles in maintaining cellular integrity and viability [14].
  • This robust SB 239063-induced neuroprotection emphasizes a significant opportunity for targeting MAPK pathways in ischemic stroke injury, and also suggests that p38 inhibition be evaluated for protective effects in other experimental models of nervous system injury and neurodegeneration [15].
  • CONCLUSIONS: These results support the notion that glutamine synthetase activity increases in response to acute hypoxic-ischemic nervous system injury in children and that other compensatory mechanisms prevail in the case of chronic hypoxic-ischemic insults [16].
  • Glial fibrillary acidic protein messenger RNA and glutamine synthetase activity after nervous system injury [17].

References

  1. Cell cycle molecules and vertebrate neuron death: E2F at the hub. Greene, L.A., Biswas, S.C., Liu, D.X. Cell Death Differ. (2004) [Pubmed]
  2. The neuroprotective potential of heat shock protein 70 (HSP70). Yenari, M.A., Giffard, R.G., Sapolsky, R.M., Steinberg, G.K. Molecular medicine today. (1999) [Pubmed]
  3. Activation of protein kinase CbetaI constitutes a new neurotrophic pathway for deafferented spiral ganglion neurons. Lallemend, F., Hadjab, S., Hans, G., Moonen, G., Lefebvre, P.P., Malgrange, B. J. Cell. Sci. (2005) [Pubmed]
  4. Role of SOCS2 in growth hormone actions. Turnley, A.M. Trends Endocrinol. Metab. (2005) [Pubmed]
  5. Amelioration of chronic neuropathic pain after partial nerve injury by adeno-associated viral (AAV) vector-mediated over-expression of BDNF in the rat spinal cord. Eaton, M.J., Blits, B., Ruitenberg, M.J., Verhaagen, J., Oudega, M. Gene Ther. (2002) [Pubmed]
  6. Response to intravenous lidocaine infusion differs based on clinical diagnosis and site of nervous system injury. Galer, B.S., Miller, K.V., Rowbotham, M.C. Neurology (1993) [Pubmed]
  7. Treatment of radiation-induced nervous system injury with heparin and warfarin. Glantz, M.J., Burger, P.C., Friedman, A.H., Radtke, R.A., Massey, E.W., Schold, S.C. Neurology (1994) [Pubmed]
  8. Upregulation of neurotoxic serine proteases, prothrombin, and protease-activated receptor 1 early after spinal cord injury. Citron, B.A., Smirnova, I.V., Arnold, P.M., Festoff, B.W. J. Neurotrauma (2000) [Pubmed]
  9. The influences of fragments and analogs of ACTH/MSH upon recovery from nervous system injury. McDaniel, W.F. Behav. Brain Res. (1993) [Pubmed]
  10. The use of lipid-coated microbubbles as a delivery agent of 7beta-hydroxycholesterol in a radiofrequency lesion in the rat brain. Wakefield, A.E., Ho, S.Y., Li, X.G., D'Arrigo, J.S., Simon, R.H. Neurosurgery (1998) [Pubmed]
  11. Mossy fiber reorganization in the epileptic hippocampus. Parent, J.M., Lowenstein, D.H. Curr. Opin. Neurol. (1997) [Pubmed]
  12. Binding characteristics of chondroitin sulfate proteoglycans and laminin-1, and correlative neurite outgrowth behaviors in a standard tissue culture choice assay. Snow, D.M., Smith, J.D., Gurwell, J.A. J. Neurobiol. (2002) [Pubmed]
  13. SB 239063, a second-generation p38 mitogen-activated protein kinase inhibitor, reduces brain injury and neurological deficits in cerebral focal ischemia. Barone, F.C., Irving, E.A., Ray, A.M., Lee, J.C., Kassis, S., Kumar, S., Badger, A.M., White, R.F., McVey, M.J., Legos, J.J., Erhardt, J.A., Nelson, A.H., Ohlstein, E.H., Hunter, A.J., Ward, K., Smith, B.R., Adams, J.L., Parsons, A.A. J. Pharmacol. Exp. Ther. (2001) [Pubmed]
  14. Hyperthermia assists survival of astrocytes from oxidative-mediated necrotic cell death. Thomas, G., Souil, E., Richard, M.J., Saunier, B., Polla, B.S., Bachelet, M. Cell. Mol. Biol. (Noisy-le-grand) (2002) [Pubmed]
  15. Inhibition of p38 mitogen-activated protein kinase provides neuroprotection in cerebral focal ischemia. Barone, F.C., Irving, E.A., Ray, A.M., Lee, J.C., Kassis, S., Kumar, S., Badger, A.M., Legos, J.J., Erhardt, J.A., Ohlstein, E.H., Hunter, A.J., Harrison, D.C., Philpott, K., Smith, B.R., Adams, J.L., Parsons, A.A. Medicinal research reviews. (2001) [Pubmed]
  16. Cerebellar glutamine synthetase in children after hypoxia or ischemia. Dao, D.N., Ahdab-Barmada, M., Schor, N.F. Stroke (1991) [Pubmed]
  17. Glial fibrillary acidic protein messenger RNA and glutamine synthetase activity after nervous system injury. Condorelli, D.F., Dell'Albani, P., Kaczmarek, L., Messina, L., Spampinato, G., Avola, R., Messina, A., Giuffrida Stella, A.M. J. Neurosci. Res. (1990) [Pubmed]
 
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