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. 2019 Feb 20;18(3):e12914. doi: 10.1111/acel.12914

Figure 4.

Figure 4

Lung endothelial cell (Ec)‐targeted p16INK4a silencing (Ec‐p16INK4a‐sil) prevents emphysema in TLR4−/− mice. (a) p16INK4a mRNA expression in Ec‐Con or Ec‐p16INK4a‐sil X WT or TLR4−/− mice. **p < 0.01, ***p < 0.001. (b) Lung compliance at 3 months of age after lung Ec‐targeted silencing of p16INK4a in TLR4−/−. **p < 0.01, ***p < 0.001, n.s.: nonsignificant. (c) Mean chord lengths from Ec‐Con or Ec‐p16INK4a‐sil X TLR4−/−. (n = 3 per group) **p < 0.01 vs. Ec‐Con X TLR4−/−. (d) H&E stained lung sections taken from Ec‐Con or Ec‐p16INK4a‐sil X TLR4−/−. Arrows point to enlarged airspaces. (e) IL‐1α and (f) IL‐6mRNA expressions in Ec‐Con or Ec‐p16INK4a‐sil X TLR4−/− mice lung. (Ec‐Con XTLR4−/− mice: n = 5, Ec‐p16INK4a‐sil X TLR4−/− mice: n = 6) *p < 0.05 vs. Ec‐Con X TLR4−/−. (g) Serum IL‐1α (n = 5) and (h) IL‐6 (n = 6) concentration in Ec‐Con or Ec‐p16INK4a‐sil X TLR4−/− mice lung **p < 0.01, ***p < 0.001 vs. Ec‐Con X TLR4−/−