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ポスター発表

第4日　5月18日（金）　　ポスター会場

4P-26　　PDF

イグラチモドが軟骨肉腫細胞の蛋白質プロファイルに与える影響

(¹聖マ医大院疾患バイオマーカー標的分子制御学・ ²聖マ医大リウマチ膠原病アレルギー内科・ ³聖マ医大院疾患プロテオーム分子病態治療学)
^o黒川真奈絵¹・ 大岡正道²・ 横山倫代³・ 有戸光美³・ 佐藤利行³・ 佐藤政秋³・ 高桑由希子²・ 表山和樹³・ 末松直也³・ 川畑仁人²・ 加藤智啓³

[Objective] To explore novel mechanisms for the effect of iguratimod (IGU) on rheumatoid arthritis (RA), we analyzed protein profile changes caused by IGU using chondrosarcoma cells.
[Methods] OUMS-27 cells were cultured in the presence or absence of 100 μM IGU. Proteins were extracted and separated by 2 dimensional-differential image gel electrophoresis (2D-DIGE). Protein spots of interest were identified by mass spectrometry.
[Results] 776 and 803 protein spots were detected in the 2D-DIGE results of 24 hour- and 6 day-treatment with IGU, respectively. In the 6 day-treatment, 22 protein spots showed 1.3-fold or higher intensity by IGU-treatment than no-treatment, whereas 15 spots showed -1.3-fold (1/1.3) or lower intensity (p<0.05). We identified 15 out of the 37 spots, which included proteins involved in packaging and splicing of pre-mRNA, regulation of signaling pathways/protein folding, innate immunity and inflammation, transcription, ATP synthesis, cytoprotection, and cytoskeleton organization. Interestingly, intensity of multiple spots of heterogenous nuclear ribonucleoprotein (hnRNP) A2/B1 and A1 was decreased by the IGU treatment, which are highly expressed in synovia of RA and/or its animal model. Specifically, hnRNP A2/B1 are known as autoantigens in RA and also as proinflammatory activators for NF-B, the target of IGU.
[Conclusion] IGU affected protein profiles of chondrosarcoma cells. The decreased expression of hnRNPs suggests novel mechanisms for anti-rheumatic effects of IGU.