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. 2022 Apr 7;14(2):245–270. doi: 10.1016/j.jcmgh.2022.04.002

Figure 6.

Figure 6

Knockout of TM9SF4 gene increased ER stress and increased apoptotic cell death in DSS-induced colitis in mice. (A) Representative immunohistochemical staining of GRP78, CHOP, and cleaved caspase 3 in colon tissues of WT and KO mice after 2% DSS treatment. Scale bars: 100 μm. Brown, immunopositive signals; blue, nuclear counterstain. (B) Representative staining of ROS (DHE staining, red), terminal deoxynucleotidyl transferase–mediated deoxyuridine triphosphate nick-end labeling (TUNEL)-positive apoptotic cells (green), and claudin-1 (green) in colon tissues of WT and KO mice after 2% DSS treatment. Scale bars: 100 μm. 4-PBA reversed the TM9SF4 knockout-induced IBD disease aggravation in (C and D) colon lengths, (E) body weight, (F) diarrhea, and (G) anal bleeding (n = 7). (H) 4-PBA reversed the TM9SF4 knockout-induced colon tissue abnormality in H&E staining–based histopathologic examination, immunostaining-based expressional change of GRP78, CHOP, and claudin-1. Brown, immunopositive signals; blue, nuclear counterstain. Scale bar: 200 μm. Means ± SEM. n = 5–7 mice per group in all experiments. ∗P < .05, ∗∗P < .01, and ∗∗∗P < .001. DAB, 3,3′-Diaminobenzidine.