Fibronectin impedes "myelin" sheet-directed flow in oligodendrocytes: A role for a beta 1 integrin-mediated PKC signaling pathway in vesicular traffickingSiskova, Z., Baron, W., de Vries, H. & Hoekstra, D., Oct-2006, In : Molecular and Cellular Neuroscience. 33, 2, p. 150-159 10 p.
Research output: Contribution to journal › Article › Academic › peer-review
Differentiation of oligodendrocytes results in the formation of the myelin sheath, a dramatic morphological alteration that accompanies cell specialization. Here, we demonstrate that changes in the extracellular micro environment may regulate these morphological changes by altering intracellular vesicular trafficking of myelin sheet-directed proteins. The data reveal that fibronectin, in contrast to laminin-2, decreased membrane-directed transport of endogenous NCAM 140 and the model viral protein VSV G, both proteins normally residing in the myelin membrane. The underlying mechanism relies on an integrin-mediated activation of PKC, which causes stable phosphorylation of MARCKS. As a result, dynamic reorganization of the cortical actin cytoskeleton necessary for the targeting of vesicular trafficking to the myelin sheet is precluded, a prerequisite for morphological differentiation. These data are discussed in the context of the demyelinating disease multiple sclerosis, i.e., that leakage of fibronectin across the blood-brain barrier may impede myelination by interference with intracellular myelin sheet-directed membrane transport. (c) 2006 Elsevier Inc. All rights reserved.
|Number of pages||10|
|Journal||Molecular and Cellular Neuroscience|
|Publication status||Published - Oct-2006|
- oligodendrocyte, ECM, integrin, MARCKS, actin, traffic, PROTEIN-KINASE-C, CULTURED OLIGODENDROCYTES, MULTIPLE-SCLEROSIS, CELL MOTILITY, MEMBRANE, DIFFERENTIATION, EXPRESSION, PDGF, ALPHA-V-BETA-3, PROLIFERATION