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      The chemokine receptor CXCR2 controls positioning of oligodendrocyte precursors in developing spinal cord by arresting their migration.

      Cell
      Animals, Animals, Newborn, Cell Communication, drug effects, physiology, Cell Death, Cell Differentiation, Cell Division, Cell Movement, Cells, Cultured, Chemokine CXCL1, Chemokines, metabolism, Chemokines, CXC, Chemotactic Factors, pharmacology, Dose-Response Relationship, Drug, Fetus, Gene Expression Regulation, Developmental, Growth Substances, Intercellular Signaling Peptides and Proteins, Mice, Mice, Knockout, Oligodendroglia, cytology, Platelet-Derived Growth Factor, Rats, Receptors, Interleukin-8B, deficiency, genetics, Signal Transduction, Spinal Cord, embryology, growth & development, Stem Cells

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          Abstract

          Spinal cord oligodendrocytes originate in the ventricular zone and subsequently migrate to white matter, stop, proliferate, and differentiate. Here we demonstrate a role for the chemokine CXCL1 and its receptor CXCR2 in patterning the developing spinal cord. Signaling through CXCR2, CXCL1 inhibited oligodendrocyte precursor migration. The migrational arrest was rapid, reversible, concentration dependent, and reflected enhanced cell/substrate interactions. White matter expression of CXCL1 was temporo-spatially regulated. Developing CXCR2 null spinal cords contained reduced oligodendrocytes, abnormally concentrated at the periphery. In slice preparations, CXCL1 inhibited embryonic oligodendrocyte precursor migration, and widespread dispersal of postnatal precursors occurred in the absence of CXCR2 signaling. These data suggest that population of presumptive white matter by oligodendrocyte precursors is dependent on localized expression of CXCL1.

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