Hypothermia treatment potentiates ERK1/2 activation after traumatic brain injury

Coleen M Atkins, Anthony A. Oliva, Ofelia F. Alonso, Shaoyi Chen, Helen Bramlett, Bing Ren Hu, W. Dalton Dietrich

Research output: Contribution to journalArticle

44 Citations (Scopus)

Abstract

Traumatic brain injury (TBI) results in significant hippocampal pathology and hippocampal-dependent memory loss, both of which are alleviated by hypothermia treatment. To elucidate the molecular mechanisms regulated by hypothermia after TBI, rats underwent moderate parasagittal fluid-percussion brain injury. Brain temperature was maintained at normothermic or hypothermic temperatures for 30 min prior and up to 4 h after TBI. The ipsilateral hippocampus was assayed with Western blotting. We found that hypothermia potentiated extracellular signal-regulated kinase 1/2 (ERK1/2) activation and its downstream effectors, p90 ribosomal S6 kinase (p90RSK) and the transcription factor cAMP response element-binding protein. Phosphorylation of another p90RSK substrate, Bad, also increased with hypothermia after TBI. ERK1/2 regulates mRNA translation through phosphorylation of mitogen-activated protein kinase-interacting kinase 1 (Mnk1) and the translation factor eukaryotic initiation factor 4E (eIF4E). Hypothermia also potentiated the phosphorylation of both Mnk1 and eIF4E. Augmentation of ERK1/2 activation and its downstream signalling components may be one molecular mechanism that hypothermia treatment elicits to improve functional outcome after TBI.

Original languageEnglish
Pages (from-to)810-819
Number of pages10
JournalEuropean Journal of Neuroscience
Volume26
Issue number4
DOIs
StatePublished - Aug 1 2007

Fingerprint

Mitogen-Activated Protein Kinase 3
Mitogen-Activated Protein Kinase 1
Hypothermia
90-kDa Ribosomal Protein S6 Kinases
Eukaryotic Initiation Factor-4E
Phosphorylation
MAP Kinase Kinase 1
Percussion
Cyclic AMP Response Element-Binding Protein
Temperature
Memory Disorders
Protein Biosynthesis
Brain Injuries
Traumatic Brain Injury
Hippocampus
Transcription Factors
Western Blotting
Pathology
Brain

Keywords

  • CREB
  • ERK1/2
  • Fluid-percussion
  • Hypothermia
  • Traumatic brain injury

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Hypothermia treatment potentiates ERK1/2 activation after traumatic brain injury. / Atkins, Coleen M; Oliva, Anthony A.; Alonso, Ofelia F.; Chen, Shaoyi; Bramlett, Helen; Hu, Bing Ren; Dalton Dietrich, W.

In: European Journal of Neuroscience, Vol. 26, No. 4, 01.08.2007, p. 810-819.

Research output: Contribution to journalArticle

Atkins, Coleen M ; Oliva, Anthony A. ; Alonso, Ofelia F. ; Chen, Shaoyi ; Bramlett, Helen ; Hu, Bing Ren ; Dalton Dietrich, W. / Hypothermia treatment potentiates ERK1/2 activation after traumatic brain injury. In: European Journal of Neuroscience. 2007 ; Vol. 26, No. 4. pp. 810-819.
@article{a30bb6e894014536aa58ac4a9a718723,
title = "Hypothermia treatment potentiates ERK1/2 activation after traumatic brain injury",
abstract = "Traumatic brain injury (TBI) results in significant hippocampal pathology and hippocampal-dependent memory loss, both of which are alleviated by hypothermia treatment. To elucidate the molecular mechanisms regulated by hypothermia after TBI, rats underwent moderate parasagittal fluid-percussion brain injury. Brain temperature was maintained at normothermic or hypothermic temperatures for 30 min prior and up to 4 h after TBI. The ipsilateral hippocampus was assayed with Western blotting. We found that hypothermia potentiated extracellular signal-regulated kinase 1/2 (ERK1/2) activation and its downstream effectors, p90 ribosomal S6 kinase (p90RSK) and the transcription factor cAMP response element-binding protein. Phosphorylation of another p90RSK substrate, Bad, also increased with hypothermia after TBI. ERK1/2 regulates mRNA translation through phosphorylation of mitogen-activated protein kinase-interacting kinase 1 (Mnk1) and the translation factor eukaryotic initiation factor 4E (eIF4E). Hypothermia also potentiated the phosphorylation of both Mnk1 and eIF4E. Augmentation of ERK1/2 activation and its downstream signalling components may be one molecular mechanism that hypothermia treatment elicits to improve functional outcome after TBI.",
keywords = "CREB, ERK1/2, Fluid-percussion, Hypothermia, Traumatic brain injury",
author = "Atkins, {Coleen M} and Oliva, {Anthony A.} and Alonso, {Ofelia F.} and Shaoyi Chen and Helen Bramlett and Hu, {Bing Ren} and {Dalton Dietrich}, W.",
year = "2007",
month = "8",
day = "1",
doi = "10.1111/j.1460-9568.2007.05720.x",
language = "English",
volume = "26",
pages = "810--819",
journal = "European Journal of Neuroscience",
issn = "0953-816X",
publisher = "Wiley-Blackwell",
number = "4",

}

TY - JOUR

T1 - Hypothermia treatment potentiates ERK1/2 activation after traumatic brain injury

AU - Atkins, Coleen M

AU - Oliva, Anthony A.

AU - Alonso, Ofelia F.

AU - Chen, Shaoyi

AU - Bramlett, Helen

AU - Hu, Bing Ren

AU - Dalton Dietrich, W.

PY - 2007/8/1

Y1 - 2007/8/1

N2 - Traumatic brain injury (TBI) results in significant hippocampal pathology and hippocampal-dependent memory loss, both of which are alleviated by hypothermia treatment. To elucidate the molecular mechanisms regulated by hypothermia after TBI, rats underwent moderate parasagittal fluid-percussion brain injury. Brain temperature was maintained at normothermic or hypothermic temperatures for 30 min prior and up to 4 h after TBI. The ipsilateral hippocampus was assayed with Western blotting. We found that hypothermia potentiated extracellular signal-regulated kinase 1/2 (ERK1/2) activation and its downstream effectors, p90 ribosomal S6 kinase (p90RSK) and the transcription factor cAMP response element-binding protein. Phosphorylation of another p90RSK substrate, Bad, also increased with hypothermia after TBI. ERK1/2 regulates mRNA translation through phosphorylation of mitogen-activated protein kinase-interacting kinase 1 (Mnk1) and the translation factor eukaryotic initiation factor 4E (eIF4E). Hypothermia also potentiated the phosphorylation of both Mnk1 and eIF4E. Augmentation of ERK1/2 activation and its downstream signalling components may be one molecular mechanism that hypothermia treatment elicits to improve functional outcome after TBI.

AB - Traumatic brain injury (TBI) results in significant hippocampal pathology and hippocampal-dependent memory loss, both of which are alleviated by hypothermia treatment. To elucidate the molecular mechanisms regulated by hypothermia after TBI, rats underwent moderate parasagittal fluid-percussion brain injury. Brain temperature was maintained at normothermic or hypothermic temperatures for 30 min prior and up to 4 h after TBI. The ipsilateral hippocampus was assayed with Western blotting. We found that hypothermia potentiated extracellular signal-regulated kinase 1/2 (ERK1/2) activation and its downstream effectors, p90 ribosomal S6 kinase (p90RSK) and the transcription factor cAMP response element-binding protein. Phosphorylation of another p90RSK substrate, Bad, also increased with hypothermia after TBI. ERK1/2 regulates mRNA translation through phosphorylation of mitogen-activated protein kinase-interacting kinase 1 (Mnk1) and the translation factor eukaryotic initiation factor 4E (eIF4E). Hypothermia also potentiated the phosphorylation of both Mnk1 and eIF4E. Augmentation of ERK1/2 activation and its downstream signalling components may be one molecular mechanism that hypothermia treatment elicits to improve functional outcome after TBI.

KW - CREB

KW - ERK1/2

KW - Fluid-percussion

KW - Hypothermia

KW - Traumatic brain injury

UR - http://www.scopus.com/inward/record.url?scp=34547978336&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=34547978336&partnerID=8YFLogxK

U2 - 10.1111/j.1460-9568.2007.05720.x

DO - 10.1111/j.1460-9568.2007.05720.x

M3 - Article

VL - 26

SP - 810

EP - 819

JO - European Journal of Neuroscience

JF - European Journal of Neuroscience

SN - 0953-816X

IS - 4

ER -