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. 2023 Feb 8;8(3):e163762. doi: 10.1172/jci.insight.163762

Figure 3. In vitro and ex vivo inhibition of antiapoptotic BCL-2 family members causes fibroblast apoptosis and to a greater degree in fibrotic fibroblasts.

Figure 3

(A) Primary lung fibroblasts from healthy and IPF donors were treated with ABT-263, and apoptosis was measured by caspase-3/7 activity. n = 3 individuals, 3–4 experimental replicates per individual. (B) PCLS from fresh healthy and IPF lungs were treated with ABT-263 and stained for anti–cleaved caspase-3 (green), α-SMA (red), and DAPI (blue) and counted for (C) total cleaved caspase-3–positive cells, (D) total α-SMA cleaved caspase-3 double-positive cells, and (E) the percentage of α-SMA+ cells that were also cleaved caspase-3 positive. n = 3 individuals, 5 images per sample were counted. White arrows indicate α-SMA/cleaved caspase-3 double-positive cells. (F) Primary lung fibroblasts from naive and 8-week silica mice were exposed to ABT-263, and apoptosis was measured by caspase-3/7 activity. n = 3–5. (G) qPCR results from in vitro–cultured fibroblasts from naive and 8-week silica mice. n = 3 per group. Graphed as scatterplot with bar, mean ± SEM. *P < 0.05, **P < 0.01, Brown-Forsythe and Welch’s ANOVA with Dunnett’s correction for multiple comparisons or 2-tailed t test with Welch’s correction.