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Chondroitin sulfates expressed on oligodendrocyte‐derived tenascin‐R are involved in neural cell recognition. Functional implications during CNS development and regeneration
Author(s) -
Probstmeier Rainer,
Stichel Christine C.,
Müller Hans Werner,
Asou Hiroaki,
Pesheva Penka
Publication year - 2000
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/(sici)1097-4547(20000401)60:1<21::aid-jnr3>3.0.co;2-h
Subject(s) - regeneration (biology) , oligodendrocyte , neuroscience , tenascin , microbiology and biotechnology , tenascin c , neural development , biology , neural stem cell , myelin , extracellular matrix , stem cell , central nervous system , biochemistry , gene , fibronectin
Abstract Tenascin‐R (TN‐R), an extracellular matrix constituent of the central nervous system (CNS), has been implicated in a variety of cell–matrix interactions underlying axon growth inhibition/guidance, myelination and neural cell migration during development and regeneration. Although most of the functional analyses have concentrated exclusively on the role of the core protein, the contribution of TN‐R glycoconjugates present on many potential sites for N ‐ and O ‐glycosylation is presently unknown. Here we provide first evidence that TN‐R derived from whole rat brain or cultured oligodendrocytes expresses chondroitin sulfate (CS) glycosaminoglycans (GAGs), i.e., C‐4S and C‐6S, that are recognized by CS‐56, a CS/dermatan sulfate‐specific monoclonal antibody. Based on different in vitro approaches utilizing substrate‐bound glycoprotein, we found that TN‐R‐linked CS GAGs (1) promote oligodendrocyte migration from white matter microexplants and increase the motility of oligodendrocyte lineage cells; (2) similar to soluble CS GAGs, induce the formation of glial scar‐like structures by cultured cerebral astrocytes; and (3) contribute to the antiadhesive properties of TN‐R for neuronal cell adhesion in an F3/F11‐independent manner, but not to neurite outgrowth inhibition, by mechanism(s) sensitive to chondroitinase or CS‐56 treatments. Furthermore, after transection of the postcommissural fornix in adult rat, CS‐bearing TN‐R was found to be stably upregulated at the lesion site. Our findings suggest the functional impact of TN‐R‐linked CS on neural cell adhesion and migration during brain morphogenesis and the contribution of TN‐R to astroglial scar formation (CS‐dependent) and axon growth inhibition (CS‐independent), i.e., suppression of axon regeneration after CNS injury. J. Neurosci. Res. 60:21–36, 2000 © 2000 Wiley‐Liss, Inc.