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Macrophage colony‐stimulating factor is expressed in neuron and microglia after focal brain injury
Author(s) -
Takeuchi Akihide,
Miyaishi Osamu,
Kiuchi Kazutoshi,
Isobe Kenichi
Publication year - 2001
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.1125
Subject(s) - microglia , macrophage colony stimulating factor , tumor necrosis factor alpha , cytokine , biology , macrophage , neuroglia , immunology , pathology , microbiology and biotechnology , chemistry , medicine , inflammation , neuroscience , in vitro , central nervous system , biochemistry
In a previous study, we have demonstrated that damaged neurons within a boundary area around necrosis fall into delayed neuronal death owing to the cytotoxic effect of microglial nitric oxide (NO), and these neurons are finally eliminated by activated microglia. In this process, microglia are activated to release NO, increase in number, and accumulate toward the damaged area. In this study, we investigated the expression of macrophage colony‐stimulating factor (M‐CSF, also called colony stimulating factor‐1; CSF‐1) and other cytokines, which are reported to relate to activation, proliferation, or migration of microglia. The mRNA of M‐CSF arose biphasically from 30 min to 1 hr and from 6 to 72 hr after the injury, as demonstrated by semiquantitative RT‐PCR. However, another cytokine of granulocyte‐macrophage CSF (GM‐CSF) or interleukin‐3 (IL‐3), which causes proliferation of microglia in vitro, was not detected. From immunohistochemical studies, positive staining of M‐CSF was observed mainly in neuron‐specific enolase (NSE)‐positive cells from 1 to 12 hr after the injury, and after that M‐CSF became positive in Griffonia simplicifolia isolectin‐B4 (GSA‐I‐B4)‐positive cells from 24 to 72 hr in the boundary area around necrosis. These results suggest that neurons around the damaged area express M‐CSF in the early phase after injury, which may initially activate microglia, and these activated microglia also express M‐CSF later, causing further proliferation or migration of microglia themselves to eliminate damaged neurons or necrotic brain tissue. J. Neurosci. Res. 65:38–44, 2001. © 2001 Wiley‐Liss, Inc.