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. Author manuscript; available in PMC: 2014 May 1.
Published in final edited form as: Gastroenterology. 2013 Jan 18;144(5):989–1000.e6. doi: 10.1053/j.gastro.2013.01.023

Figure 1.

Figure 1

Loss of P58IPK exacerbates DSS-induced colitis in mice due to a hyperactivated proapoptotic UPR. P58IPK+/− and P58IPK−/− littermates with wild-type bone marrow cells were fed 2.5% DSS in drinking water for 5 days, followed by 2 days of fresh water. (A) Body weight and (B) rectal bleeding were measured over 7 days. (C) After administration of DSS, the colons were isolated and fixed for H&E staining. Representative images are shown (original magnification 100×). (D) Histologic scores were measured in mice with DSS-induced colitis. (E) The proapoptotic transcription factor CHOP was induced whereas antiapoptotic Bcl2 was reduced in P58IPK−/− IECs. (F) IHC shows CHOP is induced in P58IPK−/− colonic epithelium with DSS-induced colitis. n = 7 for each group. *P < .05, **P < .01, ***P < .001.