Bid activates multiple mitochondrial apoptotic mechanisms in primary hepatocytes after death receptor engagement

Bradham, 1998, Mechanisms of hepatic toxicity. I. TNF-induced liver injury, Am J Physiol, 275, G387 Rust, 2000, Apoptosis and liver disease, Am J Med, 108, 567, 10.1016/S0002-9343(00)00370-3 Jaeschke, 2002, Mechanisms of hepatotoxicity, Toxicol Sci, 65, 166, 10.1093/toxsci/65.2.166 Ogasawara, 1993, Lethal effect of the anti-Fas antibody in mice, Nature, 364, 806, 10.1038/364806a0 Leist, 1994, Murine hepatocyte apoptosis induced in vitro and in vivo by TNF-alpha requires transcriptional arrest, J Immunol, 153, 1778, 10.4049/jimmunol.153.4.1778 Jaeschke, 1998, Activation of caspase 3 (CPP32)-like proteases is essential for TNF-alpha—induced hepatic parenchymal cell apoptosis and neutrophil-mediated necrosis in a murine endotoxin shock model, J Immunol, 160, 3480, 10.4049/jimmunol.160.7.3480 Ni, 1994, Fas-mediated apoptosis in primary cultured mouse hepatocytes, Exp Cell Res, 215, 332, 10.1006/excr.1994.1349 Bradham, 1998, The mitochondrial permeability transition is required for tumor necrosis factor alpha-mediated apoptosis and cytochrome c release, Mol Cell Biol, 18, 6353, 10.1128/MCB.18.11.6353 Hatano, 2000, The mitochondrial permeability transition augments Fas-induced apoptosis in mouse hepatocytes, J Biol Chem, 275, 11814, 10.1074/jbc.275.16.11814 Rodriguez, 1996, Systemic injection of a tripeptide inhibits the intracellular activation of CPP32-like proteases in vivo and fully protects mice against Fas-mediated fulminant liver destruction and death, J Exp Med, 184, 2067, 10.1084/jem.184.5.2067 Jones, 1998, Fas-mediated apoptosis in mouse hepatocytes involves the processing and activation of caspases, Hepatology, 27, 1632, 10.1002/hep.510270624 Yin, 1999, Bid-deficient mice are resistant to Fas-induced hepatocellular apoptosis, Nature, 400, 886, 10.1038/23730 Zhao, 2001, Activation of pro-death Bcl-2 family proteins and mitochondria apoptosis pathway in tumor necrosis factor-alpha-induced liver injury, J Biol Chem, 276, 27432, 10.1074/jbc.M102465200 Li, 2002, Relief of extrinsic pathway inhibition by the Bid-dependent mitochondrial release of Smac in Fas-mediated hepatocyte apoptosis, J Biol Chem, 277, 26912, 10.1074/jbc.M200726200 Desagher, 1999, Bid-induced conformational change of bax is responsible for mitochondrial cytochrome c release during apoptosis, J Cell Biol, 144, 891, 10.1083/jcb.144.5.891 Kluck, 1999, The pro-apoptotic proteins, Bid and Bax, cause a limited permeabilization of the mitochondrial outer membrane that is enhanced by cytosol, J Cell Biol, 147, 809, 10.1083/jcb.147.4.809 Kim, 2000, Bid-induced cytochrome c release is mediated by a pathway independent of mitochondrial permeability transition pore and Bax, J Biol Chem, 275, 39474, 10.1074/jbc.M003370200 Wei, 2000, tBID, a membrane-targeted death ligand, oligomerizes BAK to release cytochrome c, Genes Dev, 14, 2060, 10.1101/gad.14.16.2060 Shimizu, 2000, Proapoptotic BH3-only Bcl-2 family members induce cytochrome c release, but not mitochondrial membrane potential loss, and do not directly modulate voltage-dependent anion channel activity, Proc Natl Acad Sci U S A, 97, 577, 10.1073/pnas.97.2.577 Crompton, 1999, The mitochondrial permeability transition pore and its role in cell death, Biochem J, 341, 233, 10.1042/0264-6021:3410233 Zoratti, 1995, The mitochondrial permeability transition, Biochim Biophys Acta, 1241, 139, 10.1016/0304-4157(95)00003-A Bernardi, 1999, Mitochondria and cell death. Mechanistic aspects and methodological issues, Eur J Biochem, 264, 687, 10.1046/j.1432-1327.1999.00725.x Pastorino, 1999, Functional consequences of the sustained or transient activation by Bax of the mitochondrial permeability transition pore, J Biol Chem, 274, 31734, 10.1074/jbc.274.44.31734 Seglen, 1976, Preparation of isolated rat liver cells, Methods Cell Biol, 13, 29, 10.1016/S0091-679X(08)61797-5 Klaunig, 1981, Mouse liver cell culture. I. Hepatocyte isolation, In Vitro, 17, 913, 10.1007/BF02618288 Klaunig, 1981, Mouse liver cell culture. II. Primary culture, In Vitro, 17, 926, 10.1007/BF02618289 Hansen, 1989, Re-examination and further development of a precise and rapid dye method for measuring cell growth/cell kill, J Immunol Methods, 119, 203, 10.1016/0022-1759(89)90397-9 Nieminen, 1997, Mitochondrial permeability transition in hepatocytes induced by t-BuOOH, Am J Physiol, 272, C1286, 10.1152/ajpcell.1997.272.4.C1286 Srinivasan, 1998, Bcl-xL functions downstream of caspase-8 to inhibit Fas- and tumor necrosis factor receptor 1-induced apoptosis of MCF7 breast carcinoma cells, J Biol Chem, 273, 4523, 10.1074/jbc.273.8.4523 Mikhailov, 2001, Bcl-2 prevents bax oligomerization in the mitochondrial outer membrane, J Biol Chem, 276, 18361, 10.1074/jbc.M100655200 Waterhouse, 2001, Cytochrome c maintains mitochondrial transmembrane potential and ATP generation after outer mitochondrial membrane permeabilization during the apoptotic process, J Cell Biol, 153, 319, 10.1083/jcb.153.2.319 Yi, 2003, Inhibition of Bid-induced apoptosis by Bcl-2, J Biol Chem, 278, 16992, 10.1074/jbc.M300039200 Ashkenazi, 1998, Death receptors, Science, 281, 1305, 10.1126/science.281.5381.1305 Bajt, 2000, Protection against Fas receptor-mediated apoptosis in hepatocytes and nonparenchymal cells by a caspase-8 inhibitor in vivo, Toxicol Sci, 58, 109, 10.1093/toxsci/58.1.109 Green, 1998, Mitochondria and apoptosis, Science, 281, 1309, 10.1126/science.281.5381.1309 Kroemer, 1998, The mitochondrial death/life regulator in apoptosis and necrosis, Annu Rev Physiol, 60, 619, 10.1146/annurev.physiol.60.1.619 He, 2002, Regulated and unregulated mitochondrial permeability transition pores, FEBS Lett, 512, 1, 10.1016/S0014-5793(01)03314-2 Petronilli, 1999, Transient and long-lasting openings of the mitochondrial permeability transition pore can be monitored directly in intact cells by changes in mitochondrial calcein fluorescence, Biophys J, 76, 725, 10.1016/S0006-3495(99)77239-5 Scorrano, 2002, A distinct pathway remodels mitochondrial cristae and mobilizes cytochrome c during apoptosis, Dev Cell, 2, 55, 10.1016/S1534-5807(01)00116-2 Wei, 2001, Proapoptotic BAX and BAK, Science, 292, 727, 10.1126/science.1059108 Srinivasula, 1996, Molecular ordering of the Fas-apoptotic pathway, Proc Natl Acad Sci U S A, 93, 14486, 10.1073/pnas.93.25.14486 Stennicke, 1998, Pro-caspase-3 is a major physiologic target of caspase-8, J Biol Chem, 273, 27084, 10.1074/jbc.273.42.27084 Ichijo, 1997, Induction of apoptosis by ASK1, a mammalian MAPKKK that activates SAPK/JNK and p38 signaling pathways, Science, 275, 90, 10.1126/science.275.5296.90 Tang, 2002, The absence of NF-κB-mediated inhibition of c-Jun N-terminal kinase activation contributes to tumor necrosis factor alpha-induced apoptosis, Mol Cell Biol, 22, 8571, 10.1128/MCB.22.24.8571-8579.2002 Duan, 1997, RAIDD is a new ‘death’ adaptor molecule, Nature, 385, 86, 10.1038/385086a0 Ahmad, 1997, CRADD, a novel human apoptotic adaptor molecule for caspase-2, and FasL/tumor necrosis factor receptor-interacting protein RIP, Cancer Res, 57, 615 Pastorino, 1998, The overexpression of Bax produces cell death upon induction of the mitochondrial permeability transition, J Biol Chem, 273, 7770, 10.1074/jbc.273.13.7770 Tafani, 2000, Cytochrome c-dependent activation of caspase-3 by tumor necrosis factor requires induction of the mitochondrial permeability transition, Am J Pathol, 156, 2111, 10.1016/S0002-9440(10)65082-1 Friberg, 1998, Cyclosporin A, but not FK 506, protects mitochondria and neurons against hypoglycemic damage and implicates the mitochondrial permeability transition in cell death, J Neurosci, 18, 5151, 10.1523/JNEUROSCI.18-14-05151.1998 He, 2000, Lead and calcium produce rod photoreceptor cell apoptosis by opening the mitochondrial permeability transition pore, J Biol Chem, 275, 12175, 10.1074/jbc.275.16.12175 Heiskanen, 1999, Mitochondrial depolarization accompanies cytochrome c release during apoptosis in PC6 cells, J Biol Chem, 274, 5654, 10.1074/jbc.274.9.5654 Goldstein, 2000, The coordinate release of cytochrome c during apoptosis is rapid, complete and kinetically invariant, Nat Cell Biol, 2, 156, 10.1038/35004029