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Temporal profiles of cytoskeletal protein loss following traumatic axonal injury in mice
Journal article   Peer reviewed

Temporal profiles of cytoskeletal protein loss following traumatic axonal injury in mice

Gulyeter Serbest, Matthew F Burkhardt, Robert Siman, Ramesh Raghupathi and Kathryn E Saatman
Neurochemical research, v 32(12), pp 2006-2014
Dec 2007
PMID: 17401646

Abstract

Immunohistochemistry Mice, Inbred C57BL Axons - metabolism Male Blotting, Western Calpain - physiology Tubulin - metabolism Animals Time Factors Axons - pathology Cytoskeletal Proteins - metabolism Optic Nerve Injuries - metabolism Optic Nerve Injuries - pathology Mice Neurofilament Proteins - metabolism
To examine the time course and relative extent of proteolysis of neurofilament and tubulin proteins after traumatic axonal injury (TAI), anesthetized mice were subjected to optic nerve stretch injury. Immunohistochemistry confirmed neurofilament accumulation within axonal swellings at 4, 24, and 72 h postinjury (n = 4 injured and 2 sham per time point). Immunoblotting of optic nerve homogenates (n = 5 injured and 1 sham at 0.5, 4, 24 or 72 h) revealed calpain-mediated spectrin proteolytic fragments after injury. Protein levels for NF68 progressively decreased from 0.5 h to 24 h postinjury, while NF200 and alpha-tubulin levels decreased acutely (0.5-4 h), with a secondary decline at 72 h postinjury. These data demonstrate that diffusely distributed TAI is associated not only with a localized accumulation of neurofilament proteins, but also significant decreases in total cytoskeletal protein levels which may be mediated, in part, by calpains. Protection of the axonal cytoskeleton represents a potential therapeutic target for axonal damage associated with injury or neurodegenerative diseases.

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Collaboration types
Domestic collaboration
Web of Science research areas
Biochemistry & Molecular Biology
Neurosciences
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