noregulatory prospective of synovial mesenchymal cells, correlating with inflammatory exercise. References 1. Barr kinase inhibitor library for screening T, Carmichael NM, S?ndor GK: Juvenile idiopathic arthritis: a chronic pediatric musculoskeletal issue with major orofacial manifestations. J Can Dent Assoc 2008, 74:813 821. 2. Li X, Makarov SS: An important function of NF kappaB from the tumor like phenotype of arthritic synoviocytes. Proc Natl Acad Sci USA 2006, 103:17432 17437. P36 LC MS/MS based mostly shotgun proteomics recognized the targets of arthritis associated microRNA Riho Kurata1,2, Tomo Yonezawa1, Hideki Nakajima3, Shyuji Takada1, Hiroshi Asahara1,4,5 1Department of Methods BioMedicine, National Study Institute for Kid Health and Development, Setagaya ku, Tokyo 157 8535, Japan, 2Department of Molecular Lifestyle Sciences, Standard Medical Science and Molecular Medicine, Arthritis Analysis & Therapy 2012, Volume 14 Suppl 1 http://arthritis study.
com/supplements/14/S1 Tokai University School of Medicine, Isehara, Kanagawa, Japan, 3Department of Pediatric Hematology and Oncology Research, Nationwide Study Institute for Little one Overall health and Improvement, HSP90 inhibitors review Setagaya ku, Tokyo 157 8535, Japan, 4Department of Systems BioMedicine, Tokyo Health-related and Dental University, Bunkyo ku, Tokyo 113 8510, Japan, 5Core Analysis for Evolutional Science and Technology, Japan Science and Technology Corporation, Saitama 332 0012, Japan E mail: riho@hope. tokai u. jp Arthritis Study & Therapy 2012, 14 
36 microRNAs, which are class of post transcriptional regulators such as short 19 to 23 nucleotide non coding RNAs, complementarily bind seed sequences inside the 3 untranslational region of multiple target mRNAs, resulting in their suppression of translation or degradation.
From the former case, since the mRNA expression Lymph node 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 improvement, tumorigenesis and inflammation. We have identified enhancement of mir 146a expression in rheumatoid arthritis synoviocyte and macrophages, whilst suppression of them in osteoarthritis. Another group also have identified the enhancement of mir 146a and mir 155 in response to bacterial pathogen such as lipopolysaccaride.
Recently, mice lacking of mir 155 are resistant to collagen induced arthritis, whilst administration of mir 146a complexed with aterocollagen into joint attenuates pathological condition of CIA. These results indicate that mir 146a and mir 155 plays an important part for developing arthritis and inflammation. However, the targets of LY364947 both two miRNAs and their molecular mechanisms are not still fully recognized. 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 gi