Please use this identifier to cite or link to this item: http://hdl.handle.net/2440/62348
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Type: Journal article
Title: Genome response to tissue plasminogen activator in experimental ischemic stroke
Author: Jickling, G.
Zhan, X.
Ander, B.
Turner, R.
Stamova, B.
Xu, H.
Tian, Y.
Liu, D.
Davis, R.
Lapchak, P.
Sharp, F.
Citation: BMC Genomics, 2010; 11(1):1-10
Publisher: BioMed Central Ltd.
Issue Date: 2010
ISSN: 1471-2164
1471-2164
Statement of
Responsibility: 
Glen C Jickling, Xinhua Zhan, Bradley P Ander, Renee J Turner, Boryana Stamova, Huichun Xu, Yingfang Tian, Dazhi Liu, Ryan R Davis, Paul A Lapchak and Frank R Sharp
Abstract: Background: Tissue plasminogen activator (tPA) is known to have functions beyond fibrinolysis in acute ischemic stroke, such as blood brain barrier disruption. To further delineate tPA functions in the blood, we examined the gene expression profiles induced by tPA in a rat model of ischemic stroke. Results: tPA differentially expressed 929 genes in the blood of rats (p ≤ 0.05, fold change ≥ |1.2|). Genes identified had functions related to modulation of immune cells. tPA gene expression was found to be dependent on the reperfusion status of cerebral vasculature. The majority of genes regulated by tPA were different from genes regulated by ischemic stroke. Conclusions: tPA modulates gene expression in the blood of rats involving immune cells in a manner that is dependent on the status of vascular reperfusion. These non-fibrinolytic activities of tPA in the blood serve to better understand tPA-related complications.
Keywords: Blood-Brain Barrier; Leukocytes; Animals; Rats; Rats, Sprague-Dawley; Brain Ischemia; Tissue Plasminogen Activator; Reperfusion; Gene Expression Profiling; Male; Stroke
Rights: © 2010 Jickling et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
RMID: 0020102144
DOI: 10.1186/1471-2164-11-254
Appears in Collections:Pathology publications

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