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Volume 178, Issue 1, Pages 17-23 (September 2006)


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Oligodendrocyte precursor cells express a functional chemokine receptor CCR3: Implications for myelination

Samaneh Maysamiad1, Dan Nguyenb1, Franziska Zobelb, Sandra Heinea, Michael Höpfnerc, Martin StangeladCorresponding Author Informationemail address

Received 12 March 2006; received in revised form 23 May 2006; accepted 24 May 2006. published online 11 July 2006.

Abstract 

Myelination in the central nervous system requires an accurate interplay between oligodendrocyte precursor cells (OPC) and axons. By as yet not fully understood mechanisms, OPC proliferate, migrate to the axon to be myelinated and finally differentiate into mature oligodendrocytes. The recent finding that OPC express CXC chemokine receptors led us to the investigation of the expression and functional importance of CC chemokine receptors. Using RT-PCR, we show that primary OPC from neonatal rats express CCR3, while CCR1, CCR2, CCR4, CCR5, and CCR7 are not expressed. Immunofluorescence staining of OPC could further demonstrate protein expression of CCR3. A rise of intracellular Ca2+ upon stimulation with the appropriate ligand CCL11 showed that this receptor is functional. Moreover, CCL11 led to a concentration specific increase in proliferation, inhibition of migration, and augmentation of differentiation in primary OPC. Thus, CCR3 may influence the process of myelination. This is of general importance for both developmental tissue patterning and for repair processes in demyelinating diseases like multiple sclerosis.

a Department of Neurology, Medical School Hannover, Hannover, Germany

b Department of Neurology, Infectious Diseases and Rheumatology, Campus Benjamin Franklin, Charité, Berlin, Germany

c Medical Clinic I, Gastroenterology, Infectious Diseases and Rheumatology, Campus Benjamin Franklin, Charité, Berlin, Germany

d Center for Systems Neuroscience, Germany

Corresponding Author InformationCorresponding author. Department of Neurology, Medical School Hannover, Carl-Neuberg-Strasse 1, 30623 Hannover, Germany. Te.: +49 511 532 6676; fax: +49 511 532 3115.

1 These authors contributed equally.

PII: S0165-5728(06)00205-0

doi:10.1016/j.jneuroim.2006.05.021


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