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Liu L, Spangler LC, Prager B, et al. Spatiotemporal ablation of CXCR2 on oligodendrocyte lineage cells: Role in myelin repair. Neurol Neuroimmunol Neuroinflamm. 2015;2(6):e174doi: 10.1212/NXI.0000000000000174.
Liu, L., Spangler, L. C., Prager, B., Benson, B., Hu, B., Shi, S., Love, A., Zhang, C., Yu, M., Cotleur, A. C., & Ransohoff, R. M. (2015). Spatiotemporal ablation of CXCR2 on oligodendrocyte lineage cells: Role in myelin repair. Neurology(R) neuroimmunology & neuroinflammation, 2(6), e174. https://doi.org/10.1212/NXI.0000000000000174
Liu, LiPing, et al. "Spatiotemporal ablation of CXCR2 on oligodendrocyte lineage cells: Role in myelin repair." Neurology(R) neuroimmunology & neuroinflammation vol. 2,6 (2015): e174. doi: https://doi.org/10.1212/NXI.0000000000000174
Liu L, Spangler LC, Prager B, Benson B, Hu B, Shi S, Love A, Zhang C, Yu M, Cotleur AC, Ransohoff RM. Spatiotemporal ablation of CXCR2 on oligodendrocyte lineage cells: Role in myelin repair. Neurol Neuroimmunol Neuroinflamm. 2015 Nov 19;2(6):e174. doi: 10.1212/NXI.0000000000000174. eCollection 2015 Dec. PMID: 26668819; PMCID: PMC4676354.
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Neurol Neuroimmunol Neuroinflamm. 2015 Nov 19;2(6):e174. doi: 10.1212/NXI.0000000000000174. eCollection 2015 Dec.

Spatiotemporal ablation of CXCR2 on oligodendrocyte lineage cells: Role in myelin repair.

Neurology(R) neuroimmunology & neuroinflammation

LiPing Liu, Lisa C Spangler, Briana Prager, Bryan Benson, BingQing Hu, Samuel Shi, Anna Love, CunJin Zhang, Meigen Yu, Anne C Cotleur, Richard M Ransohoff

Affiliations

  1. Neuroinflammation Research Center (L.L., L.C.S., B.H., S.S., A.L., C.Z., M.Y., A.C.C., R.M.R.), Lerner Research Institute, Cleveland Clinic; Cleveland Clinic Lerner College of Medicine of Case Western Reserve University (B.P.); and Case Western Reserve University School of Medicine (B.B.), Cleveland, OH.

PMID: 26668819 PMCID: PMC4676354 DOI: 10.1212/NXI.0000000000000174

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.

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