Genetic ablation of Nrf2 enhances susceptibility to cigarette smoke–induced emphysema in mice
J. Clin. Invest. Tirumalai Rangasamy, et al. 114:1248 doi:10.1172/JCI21146 [Go to this article.]

Figure 3
CS treatment leads to activation of caspase-3 in Nrf2^–/– lungs. (A) Active caspase-3 expression in lung sections from CS-exposed (6 months) Nrf2^+/+ and Nrf2^–/– mice. CS-exposed Nrf2 ^–/– mice show increased numbers of caspase-3–positive cells in the alveolar septa (n = 5 per group). Magnification, ×40. (B) Number of caspase-3–positive cells in the lungs of air- and CS-exposed mice. Caspase-3–positive cells were significantly higher in the lungs of CS-exposed Nrf2^–/– mice. (C) Increased expression of the 18-kDa active form of caspase-3 in lungs of CS-exposed (6 months) Nrf2^–/– mice (Western blot; lanes 1 and 3: air- and CS-exposed Nrf2^+/+ mice, respectively; lanes 2 and 4: air- and CS-exposed Nrf2^–/– mice, respectively). (D) Quantification of procaspase-3 and active caspase-3 obtained in Western blots of air- or CS-exposed Nrf2^+/+ and Nrf2^–/– lungs. Values are represented as mean ± SEM. (E) Caspase-3 activity in the lungs of air- or CS-exposed (6 months) Nrf2^+/+ and Nrf2^–/– mice. Caspase-3 activity was significantly higher in the lungs of CS-exposed Nrf2^–/– mice than in the lungs of their wild-type counterparts (n = 3 per group). Values (relative fluorescence units [RFU]) are represented as mean ± SEM. *P – 0.05 vs. CS-exposed Nrf2^+/+ mice.