Myd88-dependent positioning of Ptgs2-expressing stromal cells maintains colonic epithelial proliferation during injury
J. Clin. Invest. Sarah L. Brown, et al. 117:258 doi:10.1172/JCI29159 [Go to this article.]

Figure 4
Exogenous dmPGE₂ rescued the rectal phenotype of DSS-treated Ptgs2^–/– and Myd88^–/– mice. (A–C) H&E-stained sections of rectums from (A) WT, (B) Ptgs2^–/–, and (C) Myd88^–/– mice that were concurrently treated with DSS and 10 μg/kg dmPGE₂. In all cases, the low-power view of the rectum was similar to that of WT DSS-treated mice in the absence of exogenous dmPGE₂ (Figure 1C). Scale bars: 100 μm. (D–F) Quantification of (D) epithelial proliferation, (E) epithelial apoptosis, and (F) crypt cell census. Mean values ± SEM were plotted for each group. An asterisk indicates a value that is statistically significantly different from the corresponding control that did not receive dmPGE₂ (*P < 0.001; Student’s t test). This dosage of dmPGE₂ did not affect the rectum of WT DSS-treated mice and rescued the rectal phenotype of DSS-treated Ptgs2^–/– and Myd88^–/– mice.