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Nogo receptor expression in microglia/macrophages during experimental autoimmune encephalomyelitis progression

Neural Regeneration Research 2018年第5期13卷 896-907页

作者： amani a.alrehaili Jae Young Lee Maha M.Bakhuraysah Min Joung Kim Pei-Mun Aui Kylie A.Magee Steven Petratos Department of Neuroscience Central Clinical School Monash University Department of Clinical Laboratories College of Applied Medical Sciences Taif University Toolgen Inc. Gasan Digital-Ro

Myelin-associated inhibitory factors within the central nervous system（CNS） are considered to be one of the main obstacles for axonal regeneration following disease or injury. The nogo receptor 1（NgR1） has been well documented to play a key role in limiting axonal regrowth in the injured and diseased mammalian CNS. However, the role of nogo receptor in immune cell activation during CNS inflammation is yet to be mechanistically elucidated. Microglia/macrophages are immune cells that are regarded as pathogenic contributors to inflammatory demyelinating lesions in multiple sclerosis（MS）. In this study, the animal model of MS, experimental autoimmune encephalomyelitis（EAE） was induced in ngr1^＋/＋ and ngr1^–/– female mice following injection with the myelin oligodendrocyte glycoprotein（MOG_（35–55）） peptide. A fatemap analysis of microglia/macrophages was performed throughout spinal cord sections of EAE-induced mice at clinical scores of 0, 1, 2 and 3, respectively（increasing locomotor disability） from both genotypes, using the CD11 b and Iba1 cell markers. Western immunoblotting using lysates from isolated spinal cord microglia/macrophages, along with immunohistochemistry and flow cytometric analysis, was performed to demonstrate the expression of nogo receptor and its two homologs during EAE progression. Myelin protein engulfment during EAE progression in ngr1^＋/＋ and ngr1^–/– mice was demonstrated by western immunblotting of lysates from isolated spinal cord microglia/macrophages, detecting levels of Nogo-A and MOG. The numbers of M1 and M2 microglia/macrophage phenotypes present in the spinal cords of EAE-induced ngr1^＋/＋ and ngr1^–/– mice, were assessed by flow cytometric analysis using CD38 and Erg-2 markers. A significant difference in microglia/macrophage numbers between ngr1^＋/＋ and ngr1^–/– mice was identified during the progression of the clinical symptoms of EAE, in the white versus gray matter regions of the spinal cord. This difference was unrelated to the expression of Ng R on these macrophage/microglial

关键词： microglia experimental autoimmune encephalomyelitis nogo receptor myelin-associated inhibitory factors （MAIFs） Nogo A neural regeneration

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Amyloid-beta-dependent phosphorylation of collapsin response mediator protein-2 dissociates kinesin in Alzheimer＇s disease

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Neural Regeneration Research 2018年第6期13卷 1066-1080页

作者： Sara H.Mokhtar Min Joung Kim Kylie A.Magee Pei Mun Aui Speros Thomas Maha M.Bakhuraysah amani a.alrehaili Jae Young Lee David L.Steer Rachel Kenny Catriona Mc Lean Michael F.Azari Antonis Birpanagos Ewlina Lipiec Philip Heraud Bayden Wood Steven Petratos Department of Neuroscience Central Clinical School Monash University Prahran Victoria Australia Department of Biochemistry and Molecular Biology Monash Universityl Clayton Victoria Australia Department of Anatomy & Developmental Biology Monash University Clayton Victoria Australia Department of Anatomical Pathology Alfred Hospital Prahran Victoria Australia School of Health and Biomedical Sciences RMIT University Bundoora Victoria Australia Division of Animal and Human Physiology Department of Biology National and Kapodistrian University of Athens Ilisia Athens Greece The Henryk Niewodniczanski Institute of Nuclear Physics Polish Academy of Sciences Department of Applied Spectroscopy RadzikowskiegoKrakow Poland Centre for Biospectroscopy and Department of Microbiology Monash University Clayton Victoria Australia

Alzheimer’s disease（AD）is a neurodegenerative disorder characterized by accumulation of amyloid plaques and neurofibrillary tangles.Prior to the development of these characteristic pathological hallmarks of AD,anterograde axonal transport is impaired.However,the key proteins that initiate these intracellular impairments remain elusive.The collapsin response mediator protein-2（CRMP-2）plays an integral role in kinesin-1-dependent axonal transport and there is evidence that phosphorylation of CRMP-2releases kinesin-1.Here,we tested the hypothesis that amyloid-beta（Aβ）-dependent phosphorylation of CRMP-2 disrupts its association with the kinesin-1（an anterograde axonal motor transport protein）in AD.We found that brain sections and lysates from AD patients demonstrated elevated phosphorylation of CRMP-2 at the T555 site.Additionally,in the transgenic Tg2576 mouse model of familial AD（FAD）that exhibits Aβaccumulation in the brain with age,we found substantial co-localization of p T555CRMP-2and dystrophic neurites.In SH-SY5Y differentiated neuronal cultures,Aβ-dependent phosphorylation of CRMP-2 at the T555 site was also elevated and this reduced the CRMP-2 association with kinesin-1.The overexpression of an unphosphorylatable form of CRMP-2 in neurons promoted the re-establishment of CRMP-2-kinesin association and axon elongation.These data suggest that Aβ-dependent phosphorylation of CRMP-2 at the T555 site may directly impair anterograde axonal transport protein function,leading to neuronal defects.

关键词： amyloid-beta protein kinases collapsin response mediator protein microtubules kinesin tubulin

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