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. 2017 Mar 27;9(5):571–588. doi: 10.15252/emmm.201606987

Figure EV4. TNBS‐induced colitis in cell‐specific DP1‐deficient mice.

Figure EV4

  1. Body weight loss, disease activity index (DAI), and colon length of DP1F/F/Tie2Cre mice, DP1F/F/VillinCre mice, DP1F/F/LysMCre mice, and DP1F/F/SM22Cre mice in response to TNBS treatment.
  2. Quantitative measurement of vascular permeability by dye leakage in the colonic mucosa from TNBS‐challenged DP1F/F/Tie2Cre and DP1F/F mice. The mice were sacrificed at day 6.
  3. TUNEL assay (left) and quantitation (right) in colonic tissues from TNBS‐challenged DP1F/F/VillinCre and DP1F/F mice. The arrows indicate the TUNEL+ cells (left). Scale bar: 100 μm. DP1F/F, n = 7; DP1F/F/VillinCre, n = 8.
  4. Representative immunofluorescent staining (left) and quantitation (right) of CD301+CD68+ cells in colonic tissues from TNBS‐challenged DP1F/F/LysMCre and DP1F/F mice. The arrows indicate the CD301+CD68+ cells (left). Scale bar: 100 μm. DP1F/F, n = 8; DP1F/F/LysMCre, n = 6.
Data information: Data are shown as mean ± SEM. Statistical significance was determined using two‐way ANOVA followed by a Bonferroni post hoc test (A) and unpaired Student's t‐tests (B–D). (A, B) *P < 0.05, **P < 0.01 compared with DP1F/F. DP1F/F, DP1F/F/Tie2Cre, DP1F/F/LysMCre, DP1F/F/SM22Cre n = 6; DP1F/F/VillinCre, n = 7. (C, D) **P < 0.01 vs. DP1F/F.