INDUCTION OF MACROPHAGE-MIGRATION INHIBITORY FACTOR MESSENGER-RIBONUCLEIC-ACID IN RAT FOREBRAIN BY REPERFUSION

Citation
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
Citations number
28
Categorie Soggetti
Surgery,"Clinical Neurology
Journal title
ISSN journal
0148396X
Volume
41
Issue
3
Year of publication
1997
Pages
648 - 653
Database
ISI
SICI code
0148-396X(1997)41:3<648:IOMIFM>2.0.ZU;2-P
Abstract
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.