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(Stroke. 2009;40:973.)
© 2009 American Heart Association, Inc.
Research Letters |
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 Peoples 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.
Correspondence to Weihong Song, MD, PhD, Townsend Family Laboratories, Department of Psychiatry, The University of British Columbia, 2255 Wesbrook Mall, Vancouver, BC V6T 1Z3, Canada. E-mail weihong{at}exchange.ubc.ca; or Shuquang Lin, MD, Guangdong Provincial Peoples Hospital, Guangzhou, China. E-mail gdpph@21cn.com
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.
Key Words: cell cultures gene regulation neurochemistry
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