| Literature DB >> 15067555 |
Masao Koda1, Yutaka Nishio, Masayuki Hashimoto, Takahito Kamada, Shuhei Koshizuka, Katsunori Yoshinaga, Shin Onodera, Jun Nishihira, Hideshige Moriya, Masashi Yamazaki.
Abstract
Macrophage migration inhibitory factor (MIF) is a multipotential protein that acts as a pro-inflammatory cytokine, pituitary hormone, immunoregulator, and mitogen. To elucidate function of MIF in spinal cord injury, we examined expression of MIF after compression-induced spinal cord injury using Northern blot analysis, in situ hybridization and immunohistochemistry. The MIF mRNA was up-regulated in injured spinal cord, peaking 3 days after injury shown by Northern blot analysis. In situ hybridization revealed up-regulation of MIF in microglia accumulating in the lesion epicenter 3 days after injury and astrocytes around the cystic cavity 1 week after injury. Double staining showed co-localization of MIF and tomato lectin in the lesioned site, indicating that microglia accumulating to the lesion epicenter express MIF. The time course of MIF expression is different from that of previous reports about cytokine expression peaking at earlier time points; thus, it is unlikely that MIF acts as a pro-inflammatory factor in the present study. The MIF may contribute to proliferation of astrocytes around the lesioned site in spinal cord injury because of its cell proliferation-promoting property.Entities:
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Year: 2004 PMID： 15067555 DOI： 10.1007/s00401-004-0853-z
Source DB: PubMed Journal: Acta Neuropathol ISSN： 0001-6322 Impact factor: 17.088