Skip to main content
. 2018 Aug;59(2):189–199. doi: 10.1165/rcmb.2017-0390OC

Figure 1.

Figure 1.

Chronic cigarette smoke (CS) exposure induces cellular senescence markers and alters expression of DNA damage response targets in mouse lung. Cellular senescence (p16 and p21) and DNA damage/repair markers (γH2AX and Ku70) in mouse lung were measured in C57BL/6J mice exposed to chronic CS. (A) Abundance of p16, p21, Ku70, and γH2AX (S139) (DNA damage) were assessed in the whole-lung homogenate by immunoblot analysis. GAPDH/β-actin was used as a loading control. (B) The band intensity was measured by densitometry, and data are shown as fold change relative to GAPDH/β-actin control. (C) Representative images of p16 expression in airway epithelium from chronic air– and CS-exposed mouse lung. Arrows indicate immunostaining for p16 dark brown color in airway epithelial cells. Insets show magnified areas. (D) Histogram for immunostaining shows the average staining score for p16 expression in the bronchial region of chronic air– and CS-exposed mouse lung determined semiquantitatively in a blinded manner. Data are shown as mean (±SEM) (n = 3–6/group). **P < 0.01 significant compared with air group control.