on January 8, 2009
Published online before print January 8, 2009, doi: 10.1161/STROKEAHA.108.530535
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Submitted on July 2, 2008
From the Department of Neurology (L.W., G.M., X.Z., S.W., C.D., J.Z.), Research Centre of Medicinal Sciences (Z.S., Q.L.), Guangdong Provincial Cardiovascular Institute (S.L.), Guangdong Provincial People's Hospital, Guangzhou, Guangdong, China; Townsend Family Laboratories (O.Z., W.S.), Department of Psychiatry, Brain Research Center, Graduate Program in Neuroscience (O.Z., W.S.), The University of British Columbia, Vancouver, BC, Canada. * To whom correspondence should be addressed. E-mail: gdpph{at}21cn.com
or weihong{at}exchange.ubc.ca.
Background and Purpose—MIF has been implicated to function in many inflammatory processes. This study examined whether MIF expression was affected in stroke and its underlying molecular mechanism. Methods—ELISA and qRT-PCR were used to detect MIF protein and mRNA in PBMCs from stroke patients, the ischemic rat brains, and controls. A MIF promoter assay under hypoxia was performed. Results—MIF protein and mRNA were significantly increased in stroke patients. Increasing levels of MIF were correlated to the severity of stroke and peaked 24 hours after stroke. MIF was significantly upregulated in focal ischemic rat brains. The activity of the human MIF promoter was significantly increased under hypoxia compared to normoxia. Conclusions—MIF gene expression is upregulated after stroke, and hypoxia signaling plays an important role in upregulation of MIF expression under stroke.
Accepted on July 27, 2008
Upregulation of Macrophage Migration Inhibitory Factor Gene Expression in Stroke
Lijuan Wang MD, PhD;
Key words: cell cultures • gene regulation • neurochemistry