About: Signaling proteins in spinal parenchyma and dorsal root ganglion in rat with spinal injury-induced spasticity     Goto   Sponge   NotDistinct   Permalink

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  • Development of progressive muscle spasticity resulting from spinal traumatic injury can be mediated by loss of local segmental inhibition and/or by an increased sensory afferent drive with resulting exacerbated α-motoneuron activity. To identify potential contributions of neuroactive substances in the development of such spasticity state, we employed a well-defined spinal injury-evoked spasticity rat model. Signaling molecules were analyzed in the spinal parenchyma below the level of spinal injury and in the corresponding dorsal root ganglion cells using Kinex antibody microarrays. The results uncovered the involvement of angiogenesis and neurodegeneration pathways together with direct cross-talk mediated by several hub proteins with SH-2 domains. At 2 and 5. weeks after transection, up-regulation of several proteins including CaMKIV, RONα and PKCδ as well as MAPK3/ERK1 phosphorylation was observed in the spinal ventral horns. Our results indicate that these signaling molecules and their neuronal effector systems cannot only play an important role in the initiation but also in the maintenance of spasticity states after spinal trauma. The exclusivity of specific protein changes observed in lumbar spinal parenchyma but not in dorsal root ganglia indicates that new treatment strategies should primarily target specific spinal segments to prevent or attenuate spasticity states.
  • Development of progressive muscle spasticity resulting from spinal traumatic injury can be mediated by loss of local segmental inhibition and/or by an increased sensory afferent drive with resulting exacerbated α-motoneuron activity. To identify potential contributions of neuroactive substances in the development of such spasticity state, we employed a well-defined spinal injury-evoked spasticity rat model. Signaling molecules were analyzed in the spinal parenchyma below the level of spinal injury and in the corresponding dorsal root ganglion cells using Kinex antibody microarrays. The results uncovered the involvement of angiogenesis and neurodegeneration pathways together with direct cross-talk mediated by several hub proteins with SH-2 domains. At 2 and 5. weeks after transection, up-regulation of several proteins including CaMKIV, RONα and PKCδ as well as MAPK3/ERK1 phosphorylation was observed in the spinal ventral horns. Our results indicate that these signaling molecules and their neuronal effector systems cannot only play an important role in the initiation but also in the maintenance of spasticity states after spinal trauma. The exclusivity of specific protein changes observed in lumbar spinal parenchyma but not in dorsal root ganglia indicates that new treatment strategies should primarily target specific spinal segments to prevent or attenuate spasticity states. (en)
Title
  • Signaling proteins in spinal parenchyma and dorsal root ganglion in rat with spinal injury-induced spasticity
  • Signaling proteins in spinal parenchyma and dorsal root ganglion in rat with spinal injury-induced spasticity (en)
skos:prefLabel
  • Signaling proteins in spinal parenchyma and dorsal root ganglion in rat with spinal injury-induced spasticity
  • Signaling proteins in spinal parenchyma and dorsal root ganglion in rat with spinal injury-induced spasticity (en)
skos:notation
  • RIV/67985904:_____/13:00395281!RIV14-TA0-67985904
http://linked.open...avai/riv/aktivita
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  • I, P(ED2.1.00/03.0124), P(ME10044), P(TA01011466)
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  • 1
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  • 105022
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  • RIV/67985904:_____/13:00395281
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  • spinal cord trauma; spasticity; hyper-reflexia (en)
http://linked.open.../riv/klicoveSlovo
http://linked.open...odStatuVydavatele
  • NL - Nizozemsko
http://linked.open...ontrolniKodProRIV
  • [A0CEA3FECBDB]
http://linked.open...i/riv/nazevZdroje
  • Journal of Proteomics
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  • 91
http://linked.open...iv/tvurceVysledku
  • Vodička, Petr
  • Gadher, S. J.
  • Hrabáková, Rita
  • Kovářová, Hana
  • Marsala, M.
  • Marsala, S.
  • Navarro, R.
  • Kupcová Skalníková, Helena
http://linked.open...ain/vavai/riv/wos
  • 000327906000004
issn
  • 1874-3919
number of pages
http://bibframe.org/vocab/doi
  • 10.1016/j.jprot.2013.06.028
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