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. 2024 Apr 9;115(6):1834–1850. doi: 10.1111/cas.16171

FIGURE 5.

FIGURE 5

AIM2‐driven LAC in Kras G12D mice is independent of inflammasome activation, yet aligns with STAT3, ERK1/2 and p38 MAPK signaling. (A) Immunoblots of individual lung lysates from Kras WT, Kras G12D, Kras G12D:Aim2 −/− and Aim2 −/− mice at 6 weeks post Ad‐Cre (Kras G12D, Kras G12D:Aim2 −/−) or PBS vehicle (Kras WT, Aim2 −/−) inhalation with indicated antibodies. (B) Densitometry of blots from (A), with expression levels relative to Tubulin loading. *p < 0.05, one‐way ANOVA. (C) ELISA for total IL‐1β protein levels in the serum of mice at 6 weeks post inhalations (n = 5/genotype). (D, F, H, J) Representative images of (D) cleaved Caspase‐1, (F) phosphorylated (p) p38 MAPK, (H) pERK1/2, and (J) pSTAT3 immunostaining of lung sections containing lesions from Kras G12D and Kras G12D:Aim2 −/− mice at 6 weeks post Ad‐Cre. Scale bars: 100 μm. (E, G, I, K) Quantification of (E) cleaved Caspase‐1, (G) pp38 MAPK, (I) pERK1/2, and (K) pSTAT3 positive cells/high‐power field (HPF) in mouse lung lesions (n = 4/genotype). *p < 0.05, **p < 0.01, ***p < 0.001, Student's t‐test.