Figure 2.

IRE1α regulates DATP number after bleomycin injury. A: RNA in situ hybridization (RNAscope) for Krt7 (teal) and Krt8 (magenta) at day 14 after bleomycin exposure and treatment with KIRA8. B: automated count of Krt7⁺ cells per 1,240-µm diameter low-power field (LPF). Each dot represents the average of 10 representative fields from one mouse with means ± SE indicated. Groups were compared by ANOVA with Fisher’s post hoc test. C: immunofluorescence staining for Krt8 (magenta) and Ager (green) at day 14 after bleomycin exposure and treatment with KIRA8. D: immunofluorescence staining as in (C) of mice with epithelial IRE1α conditional knockout (Epi^KO) or myeloid conditional knockout (Myeloid^KO). E: automated count of Krt8⁺ cells per low-power field. Each dot represents the average of eight representative fields from one mouse with means ± SE indicated. Groups were compared by ANOVA with Fisher’s post hoc test. **P < 0.01, ***P < 0.001. DATP, damage-associated transient progenitor; KIRA8, kinase inhibitor of IRE1α.