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 2
Goblet cell reorganization and loss of epithelial proliferation in the rectum of DSS-treated Ptgs2^–/– and Myd88^–/– mice. (A–F) Sections of a rectal crypt-surface unit from WT (A and B), Myd88^–/– (C and D), and Ptgs2^–/– (E and F) mice. (A, C, and E) Untreated mice. (B, D, and F) DSS-treated mice. Sections were stained with PAS/AB to identify goblet cells (left) or with goat anti-BrdU, Alexa-Fluor 594–labeled donkey anti-goat Ig (red), and bis-benzimide (blue nuclear stain) to identify cells in S-phase (right). Scale bars: 20 μm. The crypt epithelial-mesenchymal (dotted lines) and the epithelial crypt-surface junctions (dashed lines) are indicated. Quantification of goblet cells per crypt (G), crypt cell census (H), crypt height (I), epithelial apoptosis (J), and epithelial proliferation (K). Mean values ± SEM were plotted for each group. An asterisk indicates a value that is statistically significantly different from the corresponding untreated control (*P < 0.001; Student’s t test). Both DSS-treated Myd88^–/– and Ptgs2^–/– mice showed a statistically significant decrease in epithelial proliferation and crypt cell census as compared with their corresponding untreated controls.