Hypothermia treatment potentiates ERK1/2 activation after traumatic brain injury.

Hypothermia treatment potentiates ERK1/2 activation after traumatic brain injury. Research Abstract Details 

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Hypothermia treatment potentiates ERK1/2 activation after traumatic brain injury. Abstract Text:

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

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.

Hypothermia treatment potentiates ERK1/2 activation after traumatic brain injury. Publishing Authors By Initials

CM Atkins,AA Oliva,OF Alonso,S Chen,HM Bramlett,BR Hu,WD Dietrich,

For similar biological phenomena, cell phenomena, and immunity: cell physiology: cell communication: signal transduction research abstracts see: biological phenomena, cell phenomena, and immunity: cell physiology: cell communication: signal transduction research

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Hypothermia treatment potentiates ERK1/2 activation after traumatic brain injury. Journal Published:

PUBLICATION TYPE: Research Support, N.I.H., Extr

Journal: The European journal of neuroscience

VOLUME: 26

Page Numbers: 810-9

Journal Abbreviation: Eur. J. Neurosci.

ISSN: 0953-816X

DAY: 30

MONTH: 07

YEAR: 2007

Hypothermia treatment potentiates ERK1/2 activation after traumatic brain injury. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 8918110

Hypothermia treatment potentiates ERK1/2 activation after traumatic brain injury. Keywords Mesh Terms:

KEYWORDS: Signal Transduction

MESH TERMS: physiology

Chemical & Substance for Abstract: Hypothermia treatment potentiates ERK1/2 activation after traumatic brain injury. Information

Substance Name: Ribosomal Protein S6 Kinases, 90-kDa

Registry Number: EC 2.7.1.37

Grant and Affiliation Information for Hypothermia treatment potentiates ERK1/2 activation after traumatic brain injury.

AFFILIATION: Department of Neurological Surgery, University of Miami Miller School of Medicine, Miami, Florida 33136, USA.

Country: France

AGENCY: United States NINDS

GRANT: NS42133

ACRONYM: NS

MEDLINETA: Eur J Neurosci

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