Osteopontin, a macrophage-derived matricellular glycoprotein, inhibits axon outgrowth

ABSTRACT Transected axons can regenerate beyond the site of injury in the peripheral but not in the central nervous system (CNS). Increasing evidence implicates inflammatory processes as modulators of axon regeneration after injury. In this study, we addressed a possible role of the matricellular gl...

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Bibliographic Details
Published in:The FASEB journal 2005-03, Vol.19 (3), p.398-400
Main Authors: Kůry, Patrick, Zickler, Philipp, Stoll, Guido, Hartung, Hans-Peter, Jander, Sebastian
Format: Article
Language:English
Subjects:
Animals
Axons - physiology
axotomy
Cell Adhesion
Cytokines - physiology
dorsal root ganglion
extracellular matrix
Ganglia, Spinal - embryology
Ganglia, Spinal - ultrastructure
Gene Expression
Immunohistochemistry
inflammation
Kinetics
Macrophages - chemistry
Macrophages - metabolism
Nerve Crush
Nerve Regeneration - drug effects
Optic Nerve - chemistry
Optic Nerve - ultrastructure
Osteopontin
Polymerase Chain Reaction
Rats
regeneration
Sciatic Nerve - chemistry
Sciatic Nerve - ultrastructure
Sialoglycoproteins - analysis
Sialoglycoproteins - genetics
Sialoglycoproteins - physiology
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Summary:ABSTRACT Transected axons can regenerate beyond the site of injury in the peripheral but not in the central nervous system (CNS). Increasing evidence implicates inflammatory processes as modulators of axon regeneration after injury. In this study, we addressed a possible role of the matricellular glycoprotein osteopontin (OPN) using crush lesions of the optic and sciatic nerve as models of central and peripheral axotomy, respectively. OPN was strongly expressed by macrophages at the crush site in the optic but not sciatic nerve, indicating fundamental differences in the molecular programming of macrophages in both systems. Functionally, OPN exerted potent growth‐inhibitory effects in an in vitro assay of axon outgrowth. Therefore, OPN expression by lesion‐associated macrophages may contribute to the nonpermissive nature of the adult CNS preventing axonal regeneration following injury.
ISSN:0892-6638
1530-6860
DOI:10.1096/fj.04-1777fje