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. 2022 Sep 20;9:908639. doi: 10.3389/fmed.2022.908639

Figure 2.

Figure 2

Endothelial p16INK4A mediates hypoxia-induced vascular remodeling in pulmonary arterioles in the mouse lung. (A) IF images of representative pulmonary arterioles in the lungs of tamoxifen-induced p16fl/fl or p16iΔEC mice treated with normoxia or hypoxia for 3 weeks stained for αSMA, ERG, and DAPI (top) or PDGFB, ERG, and DAPI (bottom). Scale bar: 25 μm. (B) Graphs showing integrated fluorescent density of αSMA and PDGFB in tamoxifen-induced p16fl/fl or p16iΔEC mice treated with normoxia or hypoxia for 3 weeks (n = 7, mean ± SEM, *p < 0.05). (C) Graph showing Fulton's index (right ventricle/[left ventricle + septum], [RV/(LV + S)]) of tamoxifen-induced p16fl/fl or p16iΔEC mice treated with normoxia or hypoxia for 3 weeks (n = 6, mean ± SEM, *p < 0.05). (D) Graph showing right ventricular systolic pressure (RVSP) of tamoxifen-induced p16fl/fl or p16iΔEC mice treated with normoxia or hypoxia for 3 weeks (n = 5, mean ± SEM, *p < 0.05). (E) Graph showing the mRNA levels of p16INK4A in the ECs isolated from tamoxifen-induced p16fl/fl or p16iΔEC mouse lungs treated with normoxia or hypoxia for 3 weeks (n = 7–8, mean ± SEM, *p < 0.05). (F) Graphs showing the mRNA levels of αSMA and Pdgfb in the tamoxifen-induced p16fl/fl or p16iΔEC mouse lungs treated with normoxia or hypoxia for 3 weeks (n = 7–8, mean ± SEM, *p < 0.05).