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The Journal of Neuroscience, May 15, 2001, 21(10):3392-3400
Proliferation of NG2-Positive Cells and Altered Oligodendrocyte
Numbers in the Contused Rat Spinal Cord
Dana M.
McTigue,
Ping
Wei, and
Bradford T.
Stokes
Department of Physiology and Cell Biology, The Ohio State
University College of Medicine and Public Health, Columbus, Ohio 43210
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.
Key words:
myelination; spinal cord injury; astrocyte; macrophage; microglia; progenitor cell; proliferation; oligodendrocyte
Copyright © 2001 Society for Neuroscience 0270-6474/01/21103392-09$05.00/0
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