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

Authors: Kury, P  Zickler, P  Stoll, G  Hartung, HP  Jander, S 
Citation: Kury P, etal., FASEB J. 2005 Mar;19(3):398-400. Epub 2004 Dec 29.
Pubmed: (View Article at PubMed) PMID:15625076
DOI: Full-text: DOI:10.1096/fj.04-1777fje

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.

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CRRD Object Information
CRRD ID: 1581125
Created: 2006-09-18
Species: All species
Last Modified: 2006-09-18
Status: ACTIVE



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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.