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This article is part of the supplement: Proceedings of the 8th Global Arthritis Research Network (GARN) Meeting and 1st Bio-Rheumatology International Congress (BRIC)

Poster presentation

LC-MS/MS-based shotgun proteomics identified the targets of arthritis-related microRNA

Riho Kurata12*, Tomo Yonezawa1, Hideki Nakajima3, Shyuji Takada1 and Hiroshi Asahara145

Author Affiliations

1 Department of Systems BioMedicine, National Research Institute for Child Health and Development, Setagaya-ku, Tokyo 157-8535, Japan

2 Department of Molecular Life Sciences, Basic Medical Science and Molecular Medicine, Tokai University School of Medicine, Isehara, Kanagawa, Japan

3 Department of Pediatric Hematology and Oncology Research, National Research Institute for Child Health and Development, Setagaya-ku, Tokyo 157-8535, Japan

4 Department of Systems BioMedicine, Tokyo Medical and Dental University, Bunkyo-ku, Tokyo 113-8510, Japan

5 Core Research for Evolutional Science and Technology, Japan Science and Technology Corporation, Saitama 332-0012, Japan

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Arthritis Research & Therapy 2012, 14(Suppl 1):P36  doi:10.1186/ar3637


The electronic version of this article is the complete one and can be found online at: http://arthritis-research.com/content/14/S1/P36


Published:9 February 2012

© 2012 Kurata 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.

Poster presentation

microRNAs (miRNAs), which are class of post-transcriptional regulators such as short 19 to 23-nucleotide non-coding RNAs, complementarily bind seed sequences in the 3'-untranslational region of multiple target mRNAs, resulting in their suppression of translation or degradation [1]. In the former case, since the mRNA expression of the targets does not any change, transcriptomics approach, such as expression array, cannot identify the targets.

Recent studies shed light on the fine-tuning mechanism of miRNAs in myriad biological processes including development [2], tumorigenesis [3] and inflammation [4]. We have identified enhancement of mir-146a expression in rheumatoid arthritis synoviocyte and macrophages [5], whilst suppression of them in osteoarthritis [6]. Another group also have identified the enhancement of mir-146a and mir-155 in response to bacterial pathogen such as lipopolysaccaride [7]. Recently, mice lacking of mir-155 are resistant to collagen-induced arthritis (CIA) [8], whilst administration of mir-146a complexed with aterocollagen into joint attenuates pathological condition of CIA [9]. These results indicate that mir-146a and mir-155 plays an important role for developing arthritis and inflammation. However, the targets of both two miRNAs and their molecular mechanisms are not still fully identified.

In this study, in order to identify the targets of them in translational level, we established gain of function models using adenovirus- and CMV promoter-mediated overexpression in several culture models and performed liquid chromatography-tandem mass spectrometry-based shotgun proteomics in these models.

Acknowledgements

The authors sincerely thank Dr. Yanagiya R for helpful advice on preparation of adenovirus, and Dr. Inoue A for the gift of CMV vector for mir-146a.

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