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. 2020 May 23;10(3):581–599. doi: 10.1016/j.jcmgh.2020.05.004

Figure 4.

Figure 4

Gli1+fibroblasts contribute to the stroma when lineage-traced in a spontaneous pancreatic carcinogenesis model. (A) Genetic scheme for a KPF;Gli1CreERT/+;RYFP mouse. (B) Experimental design for labeling healthy Gli1+ cells before spontaneous carcinogenesis. Adult mice 5–8 weeks old were given 5 tamoxifen gavages, aged, and then harvested on evidence of disease burden. (C) IHC staining for YFP in KPF;Gli1CreERT/+;RYFP and KPF control (inset) mice. Scale bar: 100 um. (D) IF staining for YFP (green), αSMA (red), amylase (gray), and DAPI (blue); and YFP (green), podoplanin (red), E-cadherin (white), and DAPI (blue) in KPF;Gli1CreERT/+;RYFP and KPF control (inset) samples. Scale bar: 50 um. (E) Merged and single-channel IF images for YFP (green), αSMA (red), and DAPI (blue) in KF and KPF Gli1CreER;RYFP samples. Scale bar: 50 um. (F) IF quantification of the percentage of αSMA+ cells that co-expressed YFP in lineage-traced KF and KPF samples (n ≥ 5). (F) IF quantification of the percentage of YFP+ cells that co-expressed αSMA in lineage-traced KF and KPF samples (n ≥ 8). All data are expressed as means ± SEM. AMY, amylase; TAM, tamoxifen.