Wallerian degeneration and axonal regeneration after sciatic nerve crush are altered in ICAM-1-deficient mice |
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Authors: | Matthias Kirsch Marianella Campos Friz Vassilios I Vougioukas Hans-Dieter Hofmann |
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Institution: | (1) Institute of Anatomy and Cell Biology, University of Freiburg, Albertstrasse 23, 79104 Freiburg, Germany;(2) Department of Neurosurgery, University Hospital Freiburg, Breisacher Strasse 64, 79106 Freiburg, Germany;(3) Institute of Anatomy and Cell Biology, P.O. Box 111, 79001 Freiburg, Germany; |
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Abstract: | The intercellular cell adhesion molecule-1 (ICAM-1) has been implicated in the recruitment of immune cells during inflammatory
processes. Previous studies investigating its involvement in the process of Wallerian degeneration and focusing on its potential
role in macrophage recruitement have come to controversial conclusions. To examine whether Wallerian degeneration is altered
in the absence of ICAM-1, we have analyzed changes in the expression of axonal and Schwann cell markers following sciatic
nerve crush in wildtype and ICAM-1-deficient mice. We report that the lack of ICAM-1 leads to impaired axonal degeneration
and regeneration and to alterations in Schwann cell responses following sciatic nerve crush. Degradation of neurofilament
protein, the collapse of axonal profiles, and the re-expression of neurofilament proteins are substantially delayed in the
distal nerve segment of ICAM-1-/- mice. In contrast, the degradation of myelin, as determined by immunostaining for myelin protein zero, is unaltered in the
mutants. Upregulation of GAP-43 and p75 neurotrophin receptor (p75NTR) expression, characteristic for Schwann cells dedifferentiating in response to nerve injury, is differentially altered in
the mutant animals. These results indicate that ICAM-1 is essential for the normal progression of axonal degeneration and
regeneration in distal segments of injured peripheral nerves. |
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