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Osteopontin, a macrophage‐derived matricellular glycoprotein, inhibits axon outgrowth
Author(s) -
Küry Patrick,
Zickler Philipp,
Stoll Guido,
Hartung Hans-Peter,
Jander Sebastian
Publication year - 2005
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fj.04-1777fje
Subject(s) - osteopontin , axotomy , regeneration (biology) , axon , sciatic nerve , matricellular protein , microbiology and biotechnology , optic nerve , crush injury , central nervous system , lesion , periostin , macrophage , biology , pathology , neuroscience , in vitro , immunology , anatomy , medicine , extracellular matrix , surgery , biochemistry
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.