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Volume 17, Number 12, Issue of June 15, 1997 pp. 4642-4651
Copyright ©1997 Society for Neuroscience

Tenascin-R Is an Intrinsic Autocrine Factor for Oligodendrocyte Differentiation and Promotes Cell Adhesion by a SulfatideMediated Mechanism

Received Jan. 21, 1997; revised March 25, 1997; accepted April 7, 1997.

Penka Pesheva¹, Sergio Gloor³, Melitta Schachner⁴, and Rainer Probstmeier²

¹ Department of Physiology, Neurophysiology and ² Department of Biochemistry, Institute of Animal Anatomy and Physiology, University of Bonn, Bonn, Germany, and ³ Laboratory of Biochemistry and ⁴ Chair of Neurobiology, Swiss Federal Institute of Technology, 8092 Zürich, Switzerland

O4⁺ oligodendrocyte (OL) progenitors in the mammalian CNS are committed fully to terminal differentiation into myelin-forming cells. In the absence of other cell types in vitro, OL differentiation reproduces the in vivo development with a correct timing, suggesting the existence of an intrinsic regulatory mechanism that presently is unknown. We have examined the effect of two isoforms of the extracellular matrix (ECM) molecule tenascin-R (TN-R), which is expressed by OLs during the process of myelination, on the adhesion and maturation of OLs in vitro. Here we show that the substrate-bound molecules supported the adhesion of O4⁺ OLs independently of the CNS region or age from which they were derived. At the molecular level this process was mediated by protein binding to membrane surface sulfatides (Sulf), as indicated by the interference of O4 antibody and Sulf with the attachment of OLs or other Sulf⁺ cells, erythrocytes, to TN-R substrates and by direct protein-glycolipid binding studies. In the absence of platelet-derived growth factor (PDGF), exogenous TN-R induced myelin gene expression and the upregulation of its own synthesis by cultured cells, resulting in a rapid terminal differentiation of O4⁺ progenitors. Our findings strongly suggest that TN-R represents an intrinsic regulatory molecule that controls the timed OL differentiation by an autocrine mechanism and imply the relevance of TN-R for CNS myelination and remyelination.

Key words: cell adhesion; extracellular matrix; glycosphin-golipid; myelination; oligodendrocyte differentiation; sulfatide; tenascin-R

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