Essential roles of plexin-B3+ oligodendrocyte precursor cells in the pathogenesis of Alzheimer’s disease
| Autor: | Masato Hasegawa, Yoshiki Matsuda, Taeko Ito, Shuta Toru, Tadashi Kaname, Yasushi Iwasaki, Akihiko Takashima, Toshiki Uchihara, Kazuhito Satou, Yoshitaka Tatebayashi, Naomi Nihonmatsu-Kikuchi, Katsuiku Hirokawa, Xiu-Jun Yu, Akio Akagi, Mari Yoshida, Nobuyuki Ozawa |
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| Rok vydání: | 2021 |
| Předmět: |
0301 basic medicine
animal structures QH301-705.5 Central nervous system Population Medicine (miscellaneous) Brain injuries Fibroblast growth factor Article General Biochemistry Genetics and Molecular Biology Pathogenesis 03 medical and health sciences 0302 clinical medicine medicine Neurodegeneration Biology (General) education education.field_of_study biology Plexin Depolarization Alzheimer's disease Oligodendrocyte Cell biology Mechanisms of disease 030104 developmental biology medicine.anatomical_structure Gliosis embryonic structures biology.protein medicine.symptom General Agricultural and Biological Sciences 030217 neurology & neurosurgery |
| Zdroj: | Communications Biology, Vol 4, Iss 1, Pp 1-13 (2021) Communications Biology |
| ISSN: | 2399-3642 |
| DOI: | 10.1038/s42003-021-02404-7 |
| Popis: | The role of oligodendrocyte lineage cells, the largest glial population in the adult central nervous system (CNS), in the pathogenesis of Alzheimer’s disease (AD) remains elusive. Here, we developed a culture method for adult oligodendrocyte progenitor cells (aOPCs). Fibroblast growth factor 2 (FGF2) promotes survival and proliferation of NG2+ aOPCs in a serum-free defined medium; a subpopulation (~5%) of plexin-B3+ aOPCs was also found. FGF2 withdrawal decreased NG2+, but increased plexin-B3+ aOPCs and Aβ1-42 secretion. Plexin-B3+ aOPCs were distributed throughout the adult rat brain, although less densely than NG2+ aOPCs. Spreading depolarization induced delayed cortical plexin-B3+ aOPC gliosis in the ipsilateral remote cortex. Furthermore, extracellular Aβ1-42 accumulation was occasionally found around plexin-B3+ aOPCs near the lesions. In AD brains, virtually all cortical SPs were immunostained for plexin-B3, and plexin-B3 levels increased significantly in the Sarkosyl-soluble fractions. These findings suggest that plexin-B3+ aOPCs may play essential roles in AD pathogenesis, as natural Aβ-secreting cells. In order to investigate the role of oligodendrocyte lineage cells in Alzheimer’s Disease (AD) pathology, Nihonmatsu-Kikuchi et al developed a culture method for adult oligodendrocyte progenitor cells in the rat. Using this method as well as imaging AD patient brain tissue, they found that plexin-B3-expressing cells could be a potential source of amyloid β peptide. |
| Databáze: | OpenAIRE |
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