Signaling proteins in spinal parenchyma and dorsal root ganglion in rat with spinal injury-induced spasticity

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F67985904%3A_____%2F13%3A00395281" target="_blank" >RIV/67985904:_____/13:00395281 - isvavai.cz</a>

Výsledek na webu

<a href="http://dx.doi.org/10.1016/j.jprot.2013.06.028" target="_blank" >http://dx.doi.org/10.1016/j.jprot.2013.06.028</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1016/j.jprot.2013.06.028" target="_blank" >10.1016/j.jprot.2013.06.028</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Signaling proteins in spinal parenchyma and dorsal root ganglion in rat with spinal injury-induced spasticity

Popis výsledku v původním jazyce

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 ?-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 2and 5. weeks after transection, up-regulation of several proteins including CaMKIV, RON? and PKC? as well as MAPK3/ERK1 phosphorylation was observed in the spinal ventral horns. Our results indicate that these signaling molecules and the

Název v anglickém jazyce

Signaling proteins in spinal parenchyma and dorsal root ganglion in rat with spinal injury-induced spasticity

Popis výsledku anglicky

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 ?-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 2and 5. weeks after transection, up-regulation of several proteins including CaMKIV, RON? and PKC? as well as MAPK3/ERK1 phosphorylation was observed in the spinal ventral horns. Our results indicate that these signaling molecules and the

Druh

J_x - Nezařazeno - Článek v odborném periodiku (Jimp, Jsc a Jost)

CEP obor

EB - Genetika a molekulární biologie

OECD FORD obor

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Projekt

Výsledek vznikl pri realizaci vícero projektů. Více informací v záložce Projekty.

Návaznosti

I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Rok uplatnění

2013

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

Journal of Proteomics

ISSN

1874-3919

e-ISSN

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Svazek periodika

91

Číslo periodika v rámci svazku

1

Stát vydavatele periodika

NL - Nizozemsko

Počet stran výsledku

17

Strana od-do

41-57

Kód UT WoS článku

000327906000004

EID výsledku v databázi Scopus

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