title: Proliferation of NG2-positive cells and altered oligodendrocyte numbers in the contused rat spinal cord.
abstract: Given the numerous reparative roles glia may play after spinal cord injury (SCI), glial proliferation and cell number were examined in a model of traumatic SCI. Emphasis was placed on analysis of oligodendrocytes and NG2-positive (NG2+) cells, an endogenous cell population that may be involved in oligodendrocyte replacement. Overall, proliferation (assessed by bromodeoxyuridine incorporation) was markedly elevated during the first 2 weeks after injury and declined thereafter; a large portion of these dividing cells likely consisted of microglia-macrophages. Although the total number of NG2+ cells in the epicenter was reduced by half, we noted protracted proliferation in surviving NG2+ cells, with values sevenfold greater than in uninjured controls. Elevated proliferation of NG2+ cells persisted throughout the first 4 weeks after injury. However, the absolute number of NG2+ cells was not increased over controls, suggesting that the daughter cells either did not survive or they differentiated into other cell types. As expected, oligodendrocyte numbers were drastically altered after SCI. By 7 d after injury, the number of oligodendrocytes at the impact site was reduced by 93%. Despite ongoing tissue loss, the number of oligodendrocytes in spared tissue rose threefold at 14 d after injury. Although the function of NG2+ cells within the spinal cord is not completely understood, several studies suggest that they may differentiate into oligodendrocytes. Thus, proliferating NG2+ cells may contribute to the increased oligodendrocyte number observed at 2 weeks after injury. Future studies are required, however, to definitively determine the role NG2+ cells play in oligodendrocyte genesis, remyelination, and other post-injury events.
authors.affiliation: Department of Physiology and Cell Biology, The Ohio State University College of Medicine and Public Health, Columbus, Ohio 43210, USA. mctigue.2@osu.edu
authors.forename: D M
authors.initials: DM
authors.lastname: McTigue
authors.forename: P
authors.initials: P
authors.lastname: Wei
authors.forename: B T
authors.initials: BT
authors.lastname: Stokes
mesh_terms: D000818:Animals; D000941:Antigens / Q000378:metabolism*; D001253:Astrocytes / Q000378:metabolism / Q000473:pathology; D001973:Bromodeoxyuridine / Q000378:metabolism; D002452:Cell Count; D002454:Cell Differentiation; D002455:Cell Division; D004195:Disease Models, Animal; D005260:Female; D007150:Immunohistochemistry; D008264:Macrophages / Q000378:metabolism / Q000473:pathology; D017628:Microglia / Q000378:metabolism / Q000473:pathology; D009836:Oligodendroglia / Q000378:metabolism / Q000473:pathology*; D011509:Proteoglycans / Q000378:metabolism*; D051381:Rats; D011916:Rats, Inbred F344; D012583:Schwann Cells / Q000378:metabolism / Q000473:pathology; D013116:Spinal Cord / Q000378:metabolism / Q000473:pathology*; D013119:Spinal Cord Injuries / Q000378:metabolism / Q000473:pathology*; D013234:Stem Cells / Q000378:metabolism* / Q000473:pathology; D014949:Wounds, Nonpenetrating; D000099216:Chondroitin Sulfate Proteoglycan 4
chemical_list: D000941:Antigens; D001973:Bromodeoxyuridine; D011509:Proteoglycans; D000099216:Chondroitin Sulfate Proteoglycan 4