T. Yoshimoto et al., INDUCTION OF MACROPHAGE-MIGRATION INHIBITORY FACTOR MESSENGER-RIBONUCLEIC-ACID IN RAT FOREBRAIN BY REPERFUSION, Neurosurgery, 41(3), 1997, pp. 648-653
OBJECTIVE: Macrophage migration inhibitory factor (MIF) is a cytokine
that has the potential to immobilize and activate monocytes/macrophage
s. To examine whether MIF may potentially be involved in the pathogene
sis of reperfusion injury of the brain, we investigated the expression
of MIF in a rat model of reperfusion. METHODS: A four-vessel occlusio
n procedure was performed for 30 minutes using male Wistar rats to obt
ain a moderate reperfusion in the forebrains. Semiquantitatively calib
rated reverse-transcription polymerase chain reaction analysis was con
ducted to examine temporal profiles of messenger ribonucleic acid (mRN
A) expression for MIF and macrophage chemoattractant protein 1. MIF pr
otein expression was assessed with specific Western blot analysis, For
anatomic mapping of MIF, an immunohistochemical study was performed.
RESULTS: Reverse-transcription polymerase chain reaction demonstrated
that the mRNA level of MIF increased depending on the duration of repe
rfusion (less than or equal to 24 h) subsequent to global ischemia, Th
e macrophage chemoattractant protein I mRNA was also observed to incre
ase after reperfusional stress, but ifs maximum expression was reached
earlier (1 h after the stress) than was MIF mRNA, Increase of MIF pro
tein was also shown by Western blot. MIF-positive staining was observe
d in the neuronal processes (neuropil) in the cortex and basal ganglia
of a rat forebrain. CONCLUSION: This protein is up-regulated and may
modulate immunological reaction in secondary brain damage after ischem
ia and reperfusion stress.