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Neuroprotective and axon growth promoting effects of intraocular inflammation do not depend on oncomodulin or the presence of large numbers of activated macrophages.

Neuroprotective and axon growth promoting effects of intraocular inflammation do not depend on oncomodulin or the presence of large numbers of activated macrophages. Research Abstract Details 

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  • Neuroprotective and axon growth promoting effects of intraocular inflammation do not depend on oncomodulin or the presence of large numbers of activated macrophages. Abstract Text:

    thomas g haukThomas G Hauk,adrienne müllerAdrienne Müller,jieun leeJieun Lee,reto schwendenerReto Schwendener,dietmar fischerDietmar Fischer,

    Retinal ganglion cells (RGCs) cannot regenerate their axons after injury and undergo apoptosis soon after an intraorbital injury of the optic nerve. However, RGCs reactivate their axonal growth program when inflammatory reactions occur in the eye, which enables them to survive axotomy and to regenerate lengthy axons into the lesioned optic nerve. Lens injury (LI) and zymosan injections can induce these beneficial processes and provoke also a strong accumulation of activated macrophages in the vitreous body. It has recently been suggested that macrophage-derived oncomodulin is the principal mediator of this phenomenon. We show here that oncomodulin is not significantly expressed in primary macrophages and that the intraocular levels of this protein do not increase after LI or zymosan treatment. Furthermore, greatly reducing the invasion of macrophages into the inner eye does not diminish the neuroprotective effects of LI, but rather increases axon regeneration into the optic nerve. Axon regeneration is correlated with the activation of retinal astrocytes and Müller cells. Our data suggest that intraocular inflammation mediates its main beneficial effects through factors other than oncomodulin and that the underlying mechanism might be independent of the presence of activated macrophages.

    Neuroprotective and axon growth promoting effects of intraocular inflammation do not depend on oncomodulin or the presence of large numbers of activated macrophages. Publishing Authors By Initials

    tg haukTG Hauk,a müllerA Müller,j leeJ Lee,r schwendenerR Schwendener,d fischerD Fischer,

    For similar abstracts research abstracts see: abstracts research

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    Neuroprotective and axon growth promoting effects of intraocular inflammation do not depend on oncomodulin or the presence of large numbers of activated macrophages. Journal Published:

    PUBLICATION TYPE: Journal Article

    Journal: Experimental neurology

    VOLUME: 209

    Page Numbers: 469-82

    Journal Abbreviation: Exp. Neurol.

    ISSN: 0014-4886

    DAY: 29

    MONTH: 09

    YEAR: 2007

    Neuroprotective and axon growth promoting effects of intraocular inflammation do not depend on oncomodulin or the presence of large numbers of activated macrophages. Information

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    LANGUAGE: eng

    NlmUniqueID: 370712

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    Grant and Affiliation Information for Neuroprotective and axon growth promoting effects of intraocular inflammation do not depend on oncomodulin or the presence of large numbers of activated macrophages.

    AFFILIATION: Department of Experimental Neurology, University of Ulm, Albert-Einstein-Allee 11, 89081 Ulm, Germany.

    Country: United States

    United States Research PublicationUnited States Research Publication

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    MEDLINETA: Exp Neurol

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