title: Accumulation of macrophage-like cells expressing NG2 proteoglycan and Iba1 in ischemic core of rat brain after transient middle cerebral artery occlusion.
abstract: Although neurons and glia inevitably undergo degeneration in the core of ischemic lesions, many cells, particularly immune cells, infiltrate the core and survive in it. Such infiltrating cells may play certain roles in the regeneration and repair of damaged brain tissues. In this study, we characterized macrophage-like cells that accumulated in the ischemic core of a rat brain whose right middle cerebral artery was transiently occluded for 90 mins. Many of the accumulated macrophage-like cells expressed Iba1, a marker of macrophages/microglia, as well as NG2 chondroitin sulfate proteoglycan (NG2), which has been recognized as a marker of oligodendrocyte progenitor cells. Such macrophage-like cells were termed BINCs (brain Iba1(+)/NG2(+) cells) to distinguish them from NG2(-)/Iba1(+) or NG2(+)/Iba1(-) cells that were also present in the perilesion and the contralateral hemisphere. Electron microscopy showed the localization of NG2 along the plasma membrane of cells that had many phagosomes and irregular-shaped or reniform heterochromatin-rich nuclei, which are characteristics of monocytes/macrophages. Brain Iba1(+)/NG2(+) cells were highly proliferative and their number peaked at 7 days post-reperfusion. An immunoblot analysis of NG2 revealed the presence of two NG2s: one expressed by BINCs with a molecular weight of 300 kDa, and the other found in the contralateral hemisphere with a molecular weight of 290 kDa. Taken the various functions of NG2, BINCs may be involved in not only phagocytosis of degenerated cells but also the healing and regeneration of lesion cores.
authors.affiliation: Department of Neurosurgery, Graduate School of Medicine, Ehime University, Toon, Ehime, Japan.
authors.forename: Hiroaki
authors.initials: H
authors.lastname: Matsumoto
authors.forename: Yoshiaki
authors.initials: Y
authors.lastname: Kumon
authors.forename: Hideaki
authors.initials: H
authors.lastname: Watanabe
authors.forename: Takanori
authors.initials: T
authors.lastname: Ohnishi
authors.forename: Masachika
authors.initials: M
authors.lastname: Shudou
authors.forename: Miao
authors.initials: M
authors.lastname: Chuai
authors.forename: Yoshinori
authors.initials: Y
authors.lastname: Imai
authors.forename: Hisaaki
authors.initials: H
authors.lastname: Takahashi
authors.forename: Junya
authors.initials: J
authors.lastname: Tanaka
mesh_terms: D000818:Animals; D000941:Antigens / Q000096:biosynthesis*; D000943:Antigens, Differentiation / Q000096:biosynthesis; D002135:Calcium-Binding Proteins / Q000096:biosynthesis*; D002462:Cell Membrane / Q000378:metabolism / Q000648:ultrastructure; D005786:Gene Expression Regulation; D006570:Heterochromatin / Q000378:metabolism / Q000648:ultrastructure; D020244:Infarction, Middle Cerebral Artery / Q000378:metabolism* / Q000473:pathology; D008264:Macrophages / Q000378:metabolism* / Q000648:ultrastructure; D008297:Male; D008840:Microfilament Proteins; D017628:Microglia / Q000378:metabolism / Q000648:ultrastructure; D009000:Monocytes / Q000378:metabolism / Q000648:ultrastructure; D009836:Oligodendroglia / Q000378:metabolism / Q000648:ultrastructure; D010588:Phagosomes / Q000378:metabolism / Q000648:ultrastructure; D011509:Proteoglycans / Q000096:biosynthesis*; D051381:Rats; D017208:Rats, Wistar; D012038:Regeneration; D013234:Stem Cells / Q000378:metabolism / Q000648:ultrastructure; D013997:Time Factors; D000099216:Chondroitin Sulfate Proteoglycan 4
chemical_list: D000941:Antigens; D000943:Antigens, Differentiation; D002135:Calcium-Binding Proteins; D006570:Heterochromatin; D008840:Microfilament Proteins; D011509:Proteoglycans; D000099216:Chondroitin Sulfate Proteoglycan 4; C100745:Aif1 protein, rat