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Human Molecular Genetics Advance Access first published online on January 9, 2008
This version published online on January 11, 2008
Human Molecular Genetics, doi:10.1093/hmg/ddn005
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© 2007 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, The University of Sydney, Blackburn Building Level 6, Sydney, NSW 2006, Australia. 4 Department of Pathology, University of Sydney, Sydney, NSW 2006, Australia

* Correspondence: Dr Murray J Cairns, School of Biomedical Sciences, The University of Newcastle, University Drive, Callaghan, NSW 2308, Australia. Phone: 61 2 4921 8670 Fax: 61 2 4921 7903 Email: murray.cairns{at}newcastle.edu.au

Received November 1, 2007; Revised January 4, 2008; Accepted January 4, 2008

Analysis of global miRNA expression in postmortem cortical grey matter from the superior temporal gyrus (STG), revealed significant up-regulation of miR-181b expression in schizophrenia. This finding was supported by quantitative real-time RTPCR 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 (MRE) by reporter gene assay. This study suggests altered miRNA levels could be a significant factor in the dysregulation of cortical gene expression in schizophrenia.

This paper has been versioned to include figure 5.


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