Please use this identifier to cite or link to this item: http://hdl.handle.net/1959.13/922471
- Title
- MicroRNAs miR-17 and miR-20a inhibit T cell activation genes and are under-expressed in MS whole blood
- Author/Creator
-
Cox, Mathew B.;
Cairns, Murray J.;
ANZgene Multiple Sclerosis Genetics Consortium;
Gandhi, Kaushal S.;
Carroll, Adam P.;
Moscovis, Sophia;
Stewart, Graeme J.;
Broadley, Simon;
Scott, Rodney J.;
Booth, David R.;
Lechner-Scott, Jeannette
- Institution
- The University of Newcastle. Faculty of Health, School of Biomedical Sciences and Pharmacy
- Description
- It is well established that Multiple Sclerosis (MS) is an immune mediated disease. Little is known about what drives the differential control of the immune system in MS patients compared to unaffected individuals. MicroRNAs (miRNAs) are small non-coding nucleic acids that are involved in the control of gene expression. Their potential role in T cell activation and neurodegenerative disease has recently been recognised and they are therefore excellent candidates for further studies in MS. We investigated the transcriptome of currently known miRNAs using miRNA microarray analysis in peripheral blood samples of 59 treatment naive MS patients and 37 controls. Of these 59, 18 had a primary progressive, 17 a secondary progressive and 24 a relapsing remitting disease course. In all MS subtypes miR-17 and miR-20a were significantly under-expressed in MS, confirmed by RT-PCR. We demonstrate that these miRNAs modulate T cell activation genes in a knock-in and knock-down T cell model. The same T cell activation genes are also up-regulated in MS whole blood mRNA, suggesting these miRNAs or their analogues may provide useful targets for new therapeutic approaches.
- Relation
- Plos One Vol. 5, Issue 8
- Publisher Link
- http://dx.doi.org/10.1371/journal.pone.0012132
- Date
- 2010
- Publisher
- Public Library of Science
- Keyword(s)
-
Multiple Sclerosis;
microRNA;
microarray analysis;
T cell;
neurodegenerative disease
- Resource Type
- journal article
- Identifier
- http://hdl.handle.net/1959.13/922471
- Identifier
- ISSN:1932-6203
- Reviewed
-
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