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. 2019 Jun 4;33(9):9762–9774. doi: 10.1096/fj.201802519R

Figure 3.

Figure 3

Kcne2 deletion increases pulmonary damage and inflammatory cytokine production at baseline. A) Lung and blood gas parameters of Kcne2+/+ and Kcne2−/− mice as indicated. W/D of left lung sections from Kcne2+/+ and Kcne2−/− mice; n = 8–10. Partial pressure of carbon dioxide (P co2) values of Kcne2+/+ and Kcne2−/− mice; n = 6–7. Partial pressure of oxygen (P o2) values from Kcne2+/+ and Kcne2−/− mice; n = 6–7. Concentration of total oxygen (Ct o2) and concentration of total hemoglobin (CtHb) values of Kcne2+/+ and Kcne2−/− mice; n = 6–7. B) Upper, effect of Kcne2 deletion on lung histology. Lung tissues were stained with H&E and examined under a light microscope; n = 4–5 mice/genotype. Scale bar, 5 μm (a); scale bar, 20 μm (b). Lower, quantification of morphologic evaluation of lung sections of both Kcne2+/+ and Kcne2−/− mice; n = 4–5 mice/genotype. C) Left: representative micrographs of TUNEL apoptosis assay performed on lung tissue collected from Kcne2+/+ and Kcne2−/− mice. TUNEL-positive cells were stained green (TUNEL) and nuclei were stained red (DAPI). Arrows indicate TUNEL-positive cells. Right: graph showing the quantification of TUNEL-positive cells; n = 5 mice each genotype. Scale bar, 20 μm. NS, no difference between both genotypes. *P < 0.05, **P < 0.01 between genotypes.