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. 2018 Mar;188(3):586–599. doi: 10.1016/j.ajpath.2017.10.023

Figure 4.

Figure 4

miR-31-3p expression increases in ulcerative colitis (UC) tissues and experimental colitis. A: Expression of miR-31-3p in human UC tissue samples compared with control tissue samples. B: Representative images of in situ hybridization of miR-31-3p of colon tissues from UC patients and controls (arrow indicates epithelial cells). C: Expression of miR-31-3p in human Crohn disease (CD) tissue samples compared with control tissue samples is shown. D: Representative images of in situ hybridization of miR-31-3p of colon tissues from CD patients and controls (arrow indicates epithelial cells). E: Expression of miR-31-3p increases in dextran sodium sulfate (DSS) colitis. F: Representative images of in situ hybridization of miR-31-3p of colon tissues from DSS-treated C57BL6/J mice and their control counterparts (arrow indicates epithelial cells). G: Expression of miR-31-3p in colon tissues from neurokinin-1 receptor (NK-1R) knockout (KO) mice and their control counterparts [wild-type (WT) mice] in trinitrobenzene sulfonic acid (TNBS)-induced colitis. H: Representative images of in situ hybridization of miR-31-3p of colon tissues from wild-type mice with or without TNBS treatment (arrow indicates epithelial cells). Data are expressed as means ± SD. n = 14 human UC tissue samples (A); n = 10 control tissue samples (A); n = 15 human CD tissue samples (C); n = 9 control tissue samples (C); n = 8 control tissue samples (E); n = 7 DSS colitis samples (E); n = 5 (G). P > 0.05 control versus CD (C). ∗P < 0.05 versus control. Scale bars = 50 μm.