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Human Molecular Genetics Advance Access originally published online on January 9, 2008
Human Molecular Genetics 2008 17(8):1156-1168; doi:10.1093/hmg/ddn005
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© 2008 The Author(s)
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Dysregulation of miRNA 181b in the temporal cortex in schizophrenia

Natalie J. Beveridge1,2, Paul A. Tooney1,2, Adam P. Carroll1,2, Erin Gardiner1,2, Nikola Bowden1,2, Rodney J. Scott1,2, Nham Tran3, Irina Dedova1,4 and Murray J. Cairns1,2,*

1 Schizophrenia Research Institute, Sydney, NSW 2006, Australia 2 School of Biomedical Sciences, Faculty of Health, and Hunter Medical Research Institute, The University of Newcastle, University Drive, Callaghan, NSW 2308, Australia 3 Department of Infectious Diseases and Immunology 4 Department of Pathology, The University of Sydney, Blackburn Building Level 6, Sydney, NSW 2006, Australia

* To whom correspondence should be addressed. Tel: +61 249218670; Fax: +61 249217903; Email: murray.cairns{at}newcastle.edu.au

Received November 1, 2007; Accepted January 4, 2008

Analysis of global microRNA (miRNA) expression in postmortem cortical grey matter from the superior temporal gyrus, revealed significant up-regulation of miR-181b expression in schizophrenia. This finding was supported by quantitative real-time RT–PCR analysis of miRNA expression in a cohort of 21 matched pairs of schizophrenia and non-psychiatric controls. The implications of this finding are substantial, as this miRNA is predicted to regulate many target genes with potential significance to the development of schizophrenia. They include the calcium sensor gene visinin-like 1 (VSNL1) and the ionotropic AMPA glutamate receptor subunit (GRIA2), which were found to be down-regulated in the same cortical tissue from the schizophrenia group. Both of these genes were also suppressed in miR-181b transfected cells and shown to contain functional miR-181b miRNA recognition elements by reporter gene assay. This study suggests altered miRNA levels could be a significant factor in the dysregulation of cortical gene expression in schizophrenia.


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