Figure 7. Myd88-dependent alteration of PSC distribution toward the crypt base niche in response to DSS-mediated injury.
(A–D) Double-labeled 60-μm rectal sections immunofluorescently stained with Zenon Alexa Fluor 488–labeled anti-Ptgs2 Ig (PSCs, green), Cy3-labeled anti–α-SMA Ig (myofibroblasts, red), and bis-benzimide from (A) WT, (B) WT DSS-treated, (C) Myd88–/–, and (D) Myd88–/– DSS-treated mice. Arrows indicate crypt openings. (E) Quantification of PSCs per crypt-surface unit. No significant differences in the numbers of PSCs were observed when WT and Myd88–/– DSS-treated mice were compared with their untreated counterparts. AT DSS, Myd88–/– mice treated with DSS and an adoptive transfer of peripheral blood leukocytes from Rag1–/– mice. (F) Left: Map for PSC quantification in the 3 mesenchymal zones (upper, barrier associated; middle, postmitotic crypt-associated zone; lower, proliferative crypt-associated zone). Right: Quantification of PSC fractional representation (FR) for each zone. An asterisk indicates a significant difference between DSS-treated mice and untreated controls (*P < 0.05; Student’s t test). Both WT DSS-treated and Myd88–/– adoptively transferred DSS-treated mice show a significant shift in the fractional representation of PSCs toward the crypt base, while similarly treated Myd88–/– mice did not show alteration of PSC position. Scale bars: 30 μm.