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. 2010 Oct 19;183(8):1043–1054. doi: 10.1164/rccm.201002-0181OC

Figure 4.

Figure 4.

BAX or BAK are required for hyperoxia-induced cell death in primary mouse alveolar epithelial cells. (A) Mice deficient in Bak with loxP sites flanking the Bax gene Baxfl/flBak−/− were intratracheally infected with an adenovirus encoding no transgene (Ad-Null) or one encoding Cre recombinase (Ad-Cre) (1 × 109 pfu/animal) and 7 days later Cre abundance in lung homogenates was measured by immunoblotting. (B) Thirty days after infection with Ad-Null or Ad-Cre, primary ATII cells were harvested from mice and immunoblotted for the abundance of BAX (each lane represents pooled samples from four animals, densitometry represents three replicates). (C) These cells were exposed to hyperoxia for 48 hours and cell death was measured using an ELISA that detects DNA fragmentation (n = 3). *P < 0.05 for comparison with normoxic controls. †P < 0.05 for comparison of difference between Ad-Null and Ad-Cre transfected cells after exposure to hyperoxia.