TNF alpha and Fas mediate tissue damage and functional outcome after traumatic brain injury in mice.

TNF alpha and Fas mediate tissue damage and functional outcome after traumatic brain injury in mice. Research Abstract Details 

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TNF alpha and Fas mediate tissue damage and functional outcome after traumatic brain injury in mice. Abstract Text:

Daniela Bermpohl,Zerong You,Eng H Lo,Hyung-Hwan Kim,Michael J Whalen,

Tumor necrosis factor-alpha (TNFalpha) and Fas are induced after traumatic brain injury (TBI); however, their functional roles are incompletely understood. Using controlled cortical impact (CCI) and mice deficient in TNFalpha, Fas, or both (TNFalpha/Fas-/-), we hypothesized that TNFalpha and Fas receptor mediate secondary TBI in a redundant manner. Compared with wild type (WT), TNFalpha/Fas-/- mice had improved motor performance from 1 to 4 days (P<0.05), improved spatial memory acquisition at 8 to 14 days (P<0.05), and decreased brain lesion size at 2 and 6 weeks after CCI (P<0.05). Protection in TNFalpha/Fas-/- mice from histopathological and motor deficits was reversed by reconstitution with recombinant TNFalpha before CCI, and TNFalpha-/- mice administered anti-Fas ligand antibodies had improved spatial memory acquisition versus similarly treated WT mice (P<0.05). Tumor necrosis factor-alpha/Fas-/- mice had decreased the numbers of cortical cells with plasmalemma damage at 6 h (P<0.05 versus WT), and reduced matrix metalloproteinase-9 activity in injured brain at 48 and 72 h after CCI. In immature mice subjected to CCI, genetic inhibition of TNFalpha and Fas conferred beneficial effects on histopathology and spatial memory acquisition in adulthood (both P<0.05 versus WT), suggesting that the beneficial effects of TNFalpha/Fas inhibition may be permanent. The data suggest that redundant signaling pathways initiated by TNFalpha and Fas play pivotal roles in the pathogenesis of TBI, and that biochemical mechanisms downstream of TNFalpha/Fas may be novel therapeutic targets to limit neurological sequelae in children and adults with severe TBI.

TNF alpha and Fas mediate tissue damage and functional outcome after traumatic brain injury in mice. Publishing Authors By Initials

D Bermpohl,Z You,EH Lo,HH Kim,MJ Whalen,

For similar peptides: intercellular signaling peptides and proteins: cytokines: monokines: tumor necrosis factor-alpha research abstracts see: peptides: intercellular signaling peptides and proteins: cytokines: monokines: tumor necrosis factor-alpha research

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TNF alpha and Fas mediate tissue damage and functional outcome after traumatic brain injury in mice. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: Journal of cerebral blood flow and metabolism : of

VOLUME: 27

Page Numbers: 1806-18

Journal Abbreviation: J. Cereb. Blood Flow Metab.

ISSN: 0271-678X

DAY: 4

MONTH: 04

YEAR: 2007

TNF alpha and Fas mediate tissue damage and functional outcome after traumatic brain injury in mice. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 8112566

TNF alpha and Fas mediate tissue damage and functional outcome after traumatic brain injury in mice. Keywords Mesh Terms:

KEYWORDS: Tumor Necrosis Factor-alpha

MESH TERMS: physiology

Chemical & Substance for Abstract: TNF alpha and Fas mediate tissue damage and functional outcome after traumatic brain injury in mice. Information

Substance Name: Propidium

Registry Number: 36015-30-2

Grant and Affiliation Information for TNF alpha and Fas mediate tissue damage and functional outcome after traumatic brain injury in mice.

AFFILIATION: Neuroscience Center, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA 02129, USA.

Country: United States

AGENCY: United States NINDS

GRANT: R01 NS48422

ACRONYM: NS

MEDLINETA: J Cereb Blood Flow Metab

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