Abstract
Brain and spinal cord trauma have been reported to induce a variety of genes and proteins that would be expected to influence traumatic outcome [6,7,9–11,15,16,18]. Alterations in posttraumatic temperature may affect the induction of various genes in the injured tissue. Hypothermia was reported to attenuate the normal increase in interleukin-1beta RNA in traumatized rats [8]. In a model of transient global forebrain dischemia, Kamme and colleagues [12] reported that hypothermia altered the expression of specific genes. In regard to postischemic hyperthermia, Kim and colleagues [13] reported in a model of transient middle cerebral artery occlusion that c-fos and hsp70 mRNA expression were increased in heated rats when compared with normothermic animals. Because intraischemic hypothermia can significantly alter protein kinase C activity, temperature-sensitive intracellular mechanisms also participate in neuronal death [2].
This is a preview of subscription content, log in via an institution.
Buying options
Tax calculation will be finalised at checkout
Purchases are for personal use only
Learn about institutional subscriptionsReferences
Beattie MS, Shuman SL, Bresnahan JC (1998) Apoptosis and spinal cord injury. The Neuroscientist 4:163–171
Busto R, Globus MY-T, Neary JT, Ginsberg MD (1994) Regional alterations of protein kinase C activity following transient cerebral ischemia: effects of intraischemic brain temperature modulation. J Neurochem 63:1095–1103
Clark RSB, Kochanek PM, Dixon CE (1997) Early neuropathologic effects of mild or moderate hypoxemia after controlled cortical impact injury in rats. J Neuro trauma 14:179–189
Conti AC, Raghupati R, Trojanwski JO, McIntosh TK (1998) Experimental brain injury induces regionally distinct apoptosis during the acute and delayed posttraumatic period. J Neurosci 18:5663–5672
Edwards AD, Uue X, Squier MV, Thoresen M, Cady EB, Penrice J, Cooper CE, Wyatt JS, Reynolds EaR, Mehmet H (1995) Specific inhibition of apoptosis after hypoxiaischaemia by moderate post-insult hypothermia. Biochem Biophys Res Comm 217:1193–1199
Fan L, Young PR, Barone FC, Feuerstein GZ, Smith DH, Mcintosh TK (1995) Experimental brain injury induces expression of interleukin-1B mRNA in the rat brain. Molec Brain Res 30:125–130
Fan L, Young PR, Barone FC, Feuerstein GZ, Smith DH, McIntosh TK (1996) Experimental brain injury induces differential expression of tumor necrosis factor-alpha mRNA in the CNS. Molec Brain Res 36:287–291
Goss JR, Styren PO, Miller PO, Kochanek PM, Palmer DW, Marion DW, DeKosky ST (1995) Hypothermia attenuates the normal increase in interleukin-1beta RNA and nerve growth factor following traumatic brain injury in the rat. J Neurotrauma 12:159–167
Goss JR, O’Malley ME, Zou L, Styren SD, Kochanek PM, DeKosky ST (1998) Astrocytes are the major source of nerve growth factor upregulation following traumatic brain injury in the rat. Exp Neurol 149:301–309
Hayes RL, Yang K, Raghupathi R, Mcintosh TK (1995) Changes in gene expression following traumatic brain injury. J Neurotrauma 12:779–790
Hicks RR, Numan S, Dhillon HS, Prasad MR, Seroogy KB (1997) Alterations in BDNF and NT-3 mRNAs in rat hippocampus after experimental brain trauma. Molecular Brain Res 48:401–406
Kamme F, Campell K, Wieloch T (1995) Biphasic expression of the Fos and Jun families of transcription factors following transient forebrain ischaemia in the rat: effect of hypothermia. European J Neurosci 7:2007–2016
KimY, Truettner J, Zhao W, Busto R, Ginsberg MD (1998) The influence of delayed postischemic hyperthermia following transient focal ischemia: alterations of gene expression. J Neurological Sci 159:1–10
Perez-Pinzon MA, Xu GP, Born J, Lorenzo J, Busto R, Rosenthal M, Sick TJ (1999) Cytochromec is released from mitochondria into the cytosol after cerebral anoxia or ischemia. J Cereb Blood Flow Metab 19:39–43
Raghupathi R, McIntosh TK (1996) Regionally and temporally distinct patterns of induction of c-fos, c-jun, and junB mRNA following experimental brain injury in the rat. Molec Brain Res 37:134–144
Raghupathi R, Welsh FA, Lowenstein DH, Gennarelli TA, McIntosh TK (1995) Regional induction of c-fos and heat shock protein 72 mRNA following fluid-percussion brain injury in the rat. J Cereb Blood Flow Metab 15:467–473
Rink A, Fung KM, Trojanowski JQ, Lee VM-Y, Neugbauer E, McIntosh TK (1995) Evidence of apoptotic cell death after experimental traumatic brain injury in the rat. Am J Pathoi 147:1575–1583
Truettner J, Schmidt-Kastner R, Busto R, Alonso OF, Loor JY, Dietrich WD, Ginsberg MD (1999) Expression of brain-derived neurotrophic factor, nerve growth factor, and heat shock protein HSP70 following fluid percussion brain injury in rats. J Neurotrauma 16:471–486
Yakovlev AG, Knoblach SM, Fan L, Fox GB, Goodnight R, Faden AI (1997) Activation of CPT32-like caspases contribute to neuronal apoptosis and neurological dysfunction after traumatic brain injury. J Neurosci 17:7415–7424
Yenari MA, Iwayama S, Cheng D, Sun GH, Fujimura M, Morita-Fujimura Y, Chan PH, Steinberg GK (2002) Mild hypothermia attenuates cytochrome C release but does not alter Bcl-2 expression or caspase activation after experimental stroke. J Cereb Blood Flow Metals 22:29–38
Author information
Authors and Affiliations
Rights and permissions
Copyright information
© 2004 Springer Japan
About this chapter
Cite this chapter
Hayashi, N., Dietrich, D.W. (2004). Gene Expression and Apoptosis. In: Brain Hypothermia Treatment. Springer, Tokyo. https://doi.org/10.1007/978-4-431-53953-7_19
Download citation
DOI: https://doi.org/10.1007/978-4-431-53953-7_19
Publisher Name: Springer, Tokyo
Print ISBN: 978-4-431-67964-6
Online ISBN: 978-4-431-53953-7
eBook Packages: Springer Book Archive