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Tumour necrosis factor causes an increase in axonal transport of protein and demyelination in the mouse optic nerve

Identifieur interne : 000270 ( Istex/Corpus ); précédent : 000269; suivant : 000271

Tumour necrosis factor causes an increase in axonal transport of protein and demyelination in the mouse optic nerve

Auteurs : Huw G. Jenkins ; Hisako Ikeda

Source :

RBID : ISTEX:1E460BBF817D9AE0F731B027925B861DB71C1248

English descriptors

Abstract

Abstract: An increase in fast axonal transport of protein by the optic nerve was found in mice following a single combined injection of human recombinant tumour necrosis factor alpha (rTNF) and [3H]proline into the vitreous chamber. Demyelination was observed in optic nerve fibres arising from the eyes of mice which received a single rTNF injection. No such changes were detected when heat-inactivated rTNF was injected with the label. The effects of intravitreal injection of rTNF on the pathophysiology of mouse optic nerve resembled those found in mice infected with Semliki Forest virus (SFV), an animal model of multiple sclerosis. We suggest that TNF could mediate at lease some of the pathophysiological changes found in SFV-infected mice and may provide a clue concerning the disease mechanism in multiple sclerosis.

Url:
DOI: 10.1016/0022-510X(92)90194-P

Links to Exploration step

ISTEX:1E460BBF817D9AE0F731B027925B861DB71C1248

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H]proline into the vitreous chamber. Demyelination was observed in optic nerve fibres arising from the eyes of mice which received a single rTNF injection. No such changes were detected when heat-inactivated rTNF was injected with the label. The effects of intravitreal injection of rTNF on the pathophysiology of mouse optic nerve resembled those found in mice infected with Semliki Forest virus (SFV), an animal model of multiple sclerosis. We suggest that TNF could mediate at lease some of the pathophysiological changes found in SFV-infected mice and may provide a clue concerning the disease mechanism in multiple sclerosis.</ce:simple-para>
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<ce:section-title>Keywords</ce:section-title>
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<ce:text>Axonal transport</ce:text>
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<ce:text>Cytokine</ce:text>
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<ce:text>Demyelination</ce:text>
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<ce:text>Optic nerve</ce:text>
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<ce:keyword>
<ce:text>Retina</ce:text>
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<ce:text>Tumour necrosis factor</ce:text>
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<namePart type="given">Huw G.</namePart>
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<description>Correspondence to: H.G. Jenkins, The Vision Research Unit, The Rayne Institute, St. Thomas' Hospital, London, SE1 7EH, U.K.. Tel: (44)(71) 928-9292, ext. 3407; Fax: (44)(71) 922-8079.</description>
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<abstract lang="en">Abstract: An increase in fast axonal transport of protein by the optic nerve was found in mice following a single combined injection of human recombinant tumour necrosis factor alpha (rTNF) and [3H]proline into the vitreous chamber. Demyelination was observed in optic nerve fibres arising from the eyes of mice which received a single rTNF injection. No such changes were detected when heat-inactivated rTNF was injected with the label. The effects of intravitreal injection of rTNF on the pathophysiology of mouse optic nerve resembled those found in mice infected with Semliki Forest virus (SFV), an animal model of multiple sclerosis. We suggest that TNF could mediate at lease some of the pathophysiological changes found in SFV-infected mice and may provide a clue concerning the disease mechanism in multiple sclerosis.</abstract>
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<topic>Axonal transport</topic>
<topic>Cytokine</topic>
<topic>Demyelination</topic>
<topic>Optic nerve</topic>
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