Inhibition of Epidermal Growth Factor Receptor Improves Myelination and Attenuates Tissue Damage of Spinal Cord Injury |
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Authors: | Si Zhang Peijun Ju Editha Tjandra Yeeshan Yeap Hamed Owlanj Zhiwei Feng |
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Affiliation: | 1.School of Life Science and Technology,Xinxiang Medical University,Xinxiang,China;2.Brain Research Center, Faculty of Medicine,University of British Columbia,Vancouver,Canada;3.Shanghai Key Laboratory of Psychotic Disorders, Shanghai Mental Health Center,Shanghai Jiao Tong University School of Medicine,Shanghai,China;4.School of Biological Sciences,Nanyang Technological University,Singapore,Singapore;5.Cytogenetics Laboratory,Singapore General Hospital,Singapore,Singapore |
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Abstract: | Preventing demyelination and promoting remyelination of denuded axons are promising therapeutic strategies for spinal cord injury (SCI). Epidermal growth factor receptor (EGFR) inhibition was reported to benefit the neural functional recovery and the axon regeneration after SCI. However, its role in de- and remyelination of axons in injured spinal cord is unclear. In the present study, we evaluated the effects of EGFR inhibitor, PD168393 (PD), on the myelination in mouse contusive SCI model. We found that expression of myelin basic protein (MBP) in the injured spinal cords of PD treated mice was remarkably elevated. The density of glial precursor cells and oligodendrocytes (OLs) was increased and the cell apoptosis in lesions was attenuated after PD168393 treatment. Moreover, PD168393 treatment reduced both the numbers of OX42 + microglial cells and glial fibrillary acidic protein + astrocytes in damaged area of spinal cords. We thus conclude that the therapeutic effects of EGFR inhibition after SCI involves facilitating remyelination of the injured spinal cord, increasing of oligodendrocyte precursor cells and OLs, as well as suppressing the activation of astrocytes and microglia/macrophages. |
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