TRAIL receptor–mediated JNK activation and Bim phosphorylation critically regulate Fas-mediated liver damage and lethality
J. Clin. Invest. Nadia Corazza, et al. 116:2493 doi:10.1172/JCI27726 [Go to this article.]

Figure 2
Attenuated Fas-induced liver damage inTRAIL -deficient mice. Wild-type or TRAIL-deficient mice were injected i.v. with PBS as a control or anti-Fas antibody. Liver tissue and serum samples of mice still alive after 4 hours were isolated and analyzed. (A) Macroscopic analysis of intact liver from untreated wild-type (TRAIL^+/+) mice and anti-Fas–injected wild-type and TRAIL-deficient (TRAIL^–/–) mice. The liver of anti-Fas–treated wild-type mice is hemorrhagic and necrotic. (B) Serum levels of liver transaminase (AST) in control (PBS) or anti-Fas–treated wild-type or TRAIL-deficient mice. One representative experiment out of 3 is shown. n = 4 mice per group, mean ± SD. *P < 0.01, Student’s t test. (C) Histological analysis of liver sections from untreated wild-type (TRAIL^+/+, control), anti-Fas–treated wild-type, and TRAIL-deficient mice. Low- and high-power magnification of representative samples is shown. (D) Immunohistochemistry for active caspase 3 (Casp 3). Caspase 3–positive apoptotic cells are stained in red. (E) Detection of caspase 3 activation in control-treated or anti-Fas–treated liver samples from wild-type or TRAIL-deficient mice by Western blot. The 18-kDa fragment indicates caspase cleavage and activation. Samples from 1 control and 4 anti-Fas–treated mice are shown.