GLIAL CELLSModulation of rat oligodendrocyte precursor cells by the chemokine CXCL12Maysami, Samaneha b; Nguyen, Danc; Zobel, Franziskac; Pitz, Carolinea; Heine, Sandraa; Höpfner, Michaeld; Stangel, Martina b Author Information aDepartment of Neurology, Medical School Hannover bCenter for Systems Neuroscience, Hannover cDepartment of Neurology and dMedical Clinic I, Gastroenterology, Infectious Diseases and Rheumatology, Campus Benjamin Franklin, Charité, Berlin, Germany Correspondence and requests for reprints to PD Dr Martin Stangel, Department of Neurology, Medical School Hannover, Carl-Neuberg-Strasse 1 30625 Hannover, Germany Tel: +49 511 532 6676; fax: +49 511 532 3115; e-mail: [email protected] Sponsorship: This study was supported by the DFG (SFB 566) and the Gemeinnützige Hertiestiftung. Received 2 May 2006; revised 14 May 2006; accepted 15 May 2006 NeuroReport: July 31, 2006 - Volume 17 - Issue 11 - p 1187-1190 doi: 10.1097/01.wnr.0000227985.92551.9a Buy Metrics Abstract Migration, proliferation, and differentiation of oligodendrocyte precursor cells are essential for the assembly of myelin in the central nervous system. Knowledge on the regulation of these precursor cells is therefore of great importance for the understanding of developmental myelination and remyelination in demyelinating diseases. Here, we show that primary rat oligodendrocyte precursor cells express the chemokine receptor CXCR4. Stimulation with the ligand CXCL12 (SDF-1α) leads to intracellular Ca2+ elevation. Furthermore, 10 ng/ml CXCL12 augmented differentiation of precursors into mature oligodendrocytes. Migration toward growth factor conditioned medium was inhibited by CXCL12, while proliferation was only slightly modulated. The effect of CXCL12 on both migration and differentiation was blocked using a G protein antagonist. These data suggest a role for CXCL12 and oligodendroglial CXCR4 receptors during developmental myelination and repair in demyelinating diseases of the central nervous system. © 2006 Lippincott Williams & Wilkins, Inc.