Spatiotemporal ablation of CXCR2 on oligodendrocyte lineage cells: Role in myelin repair. Issue 6 (December 2015)

• Record Type: Journal Article
• Authors: Liu, LiPing; Spangler, Lisa C.; Prager, Briana; Benson, Bryan; Hu, BingQing; Shi, Samuel; Love, Anna; Zhang, CunJin; Yu, Meigen; Cotleur, Anne C.; Ransohoff, Richard M.
• Is Part Of: Neurology. Volume 2:Issue 6(2015)
• Publication Date: 2015-12
• Subjects: Neuroimmunology -- Periodicals; Neurology -- Periodicals; 616.8
• DOI: 10.1212/NXI.0000000000000174
• Languages: English
• ISSNs: 2332-7812

Abstract

Abstract : Background: Residual CXCR2 expression on CNS cells in Cxcr2 +/− → Cxcr2 −/− chimeric animals slowed remyelination after both experimental autoimmune encephalomyelitis and cuprizone-induced demyelination. Methods: We generated Cxcr2 fl/− :PLPCre-ER(T) mice enabling an inducible, conditional deletion of Cxcr2 on oligodendrocyte lineage cells of the CNS. Cxcr2 fl/− :PLPCre-ER(T) mice were evaluated in 2 demyelination/remyelination models: cuprizone-feeding and in vitro lysophosphatidylcholine (LPC) treatment of cerebellar slice cultures. Results: Cxcr2 fl/− :PLPCre-ER(T) + (termed Cxcr2 -cKO) mice showed better myelin repair 4 days after LPC-induced demyelination of cerebellar slice cultures. Cxcr2 -cKOs also displayed enhanced hippocampal remyelination after a 2-week recovery from 6-week cuprizone feeding. Conclusion: Using 2 independent demyelination/remyelination models, our data document enhanced myelin repair in Cxcr2 -cKO mice, consistent with the data obtained from radiation chimerism studies of germline CXCR2. Further experiments are appropriate to explore how CXCR2 function in the oligodendrocyte lineage accelerates myelin repair.