We have focused on detecting miRNAs related to ulcerative colitis of mouse, identifying their target molecules, and analyzing the correlation between the miRNAs and their target genes in colon cell lines. Methods: UC-associated Idasanutlin ic50 miRNAs were identified by miRNA microarray analysis of UC colon tissues and normal colon tissues of mouse. The results were validated by quantitative RT-qPCR. MIR429 target genes

were identified by the mRNAs downregulated in MIR429-overexpressing cells (determined by mRNA microarray analysis). Luciferase reporter plasmids were constructed to confirm the effect of MIR429 on target gene expression. The protein expression of the target genes was measured by western blot. Results: Thirty-seven miRNAs were identified as UC-associated miRNAs. We investigated one, MIR429,

which was specifically downregulated in UC, and identified 41 genes as targets of MIR429. The association between MIR429 and CHMP5 was verified in this study. CHMP5 transcript expression was directly downregulated by MIR429; protein expression was also downregulated. Conclusion: Our results suggest that MIR429 could play an important role in the pathogenesis of ulcerative colitis. Key Word(s): Na Presenting Author: NAZRI MUSTAFFA Additional Authors: WON FEN WONG, ALICIA YILING PHAN, IDA HILMI, KHEAN LEE GOH Corresponding Author: NAZRI MUSTAFFA Affiliations: University of Malaya, University of Malaya, University of Malaya, University of Malaya Objective: Gut inflammation mTOR inhibitor in Crohn’s disease (CD) is related to T-helper type 1 (Th1) cells, with high levels of interferon (IFN)-γ being produced. Th17 cells are also involved, identified by the production of interleukin (IL)-17; IL-6 drives early Th17 cell differentiation. IL-17′s role in the pathogenesis of CD however has not been definitely confirmed. We thus set out to identify the relationship of IFN-γ, IL-6 and IL-17 to disease activity in a cohort of CD patients from the University Malaya Medical Centre. Methods: Serum from blood samples of CD patients and

control subjects were obtained from 1:2 diluted supernatant following Ficoll-Paque density centrifugation. Serum IFN-γ, IL-6, and IL-17 concentrations were measured using ELISA kits (Biolegend, USA). Clinical 上海皓元 disease activity was measured using the Harvey-Bradshaw Index. Results: A total of 24 CD patients (16 in remission, 6 having active disease) and 9 control subjects were recruited. Compared to controls, for CD patients in remission IFN-γ was not significantly raised (p = 0.08) while there was a significant rise in patients with active disease (p < 0.05). IL-6 was raised in both groups of CD patients (p < 0.01 for those in remission and p < 0.01 with active disease). IL-17 however was not increased in both groups of CD patients (p = 0.11 for patients in remission, and p = 0.07 for those with active disease).