ArticleHepatology (Baltimore, Md.)2009
The strength of the Fas ligand signal determines whether hepatocytes act as type 1 or type 2 cells in murine livers.
Article in Hepatology (Baltimore, Md.), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
17 citing papers in PubMed, 40 citations in OpenAlex.
- Isolation, culture, and delivery considerations for the use of mesenchymal stem cells in potential therapies for acute liver failure.Frontiers in immunology · 2023Review
- Mito-tempo protects against acute liver injury but induces limited secondary apoptosis during the late phase of acetaminophen hepatotoxicity.Archives of toxicology · 2019Article
- The role of apoptosis in acetaminophen hepatotoxicity.Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association · 2018Review
- Caspase inhibitors for the treatment of liver disease: friend or foe?Expert review of gastroenterology & hepatology · 2017Article
- Balance between short and long isoforms of cFLIP regulates Fas-mediated apoptosis in vivo.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Experimental models of hepatotoxicity related to acute liver failure.Toxicology and applied pharmacology · 2016Review
- Xenobiotic and Endobiotic Mediated Interactions Between the Cytochrome P450 System and the Inflammatory Response in the Liver.Advances in pharmacology (San Diego, Calif.) · 2015Review
- Regulation of TRAIL-receptor expression by the ubiquitin-proteasome system.International journal of molecular sciences · 2014Review
- Differential regulation of inflammation and apoptosis in Fas-resistant hepatocyte-specific Bid-deficient mice.Journal of hepatology · 2014Article
- pERK 1/2 inhibit Caspase-8 induced apoptosis in cancer cells by phosphorylating it in a cell cycle specific manner.Molecular oncology · 2014Article
- Rejuvenating Bi(d)ology.Oncogene · 2013Review
- Apoptosis and necrosis in the liver.Comprehensive Physiology · 2013Review
- Clinical targeting of the TNF and TNFR superfamilies.Nature reviews. Drug discovery · 2013Review
- Fas death receptor signalling: roles of Bid and XIAP.Cell death and differentiation · 2012Review
- PMLRARα binds to Fas and suppresses Fas-mediated apoptosis through recruiting c-FLIP in vivo.Blood · 2011Article
- Pro- and anti-apoptotic CD95 signaling in T cells.Cell communication and signaling : CCS · 2011Article
- Hepatocyte death: a clear and present danger.Physiological reviews · 2010Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 3 countries.
Funding
Abstract
unlabelledThe BH3-interacting domain death agonist Bid has been shown to be critical for Fas-induced hepatocellular apoptosis. Furthermore, some studies have suggested that phosphorylation of Bid may determine its apoptotic function and may act as a switch to nonapoptotic functions. The aim of this study was to evaluate the role of Bid and phosphorylated Bid for Fas ligand (FasL)-induced apoptosis in murine livers. The monoclonal antibody Jo2 and a hexameric form of sFasL (MegaFasL) were used to induce apoptosis in wild-type, Bid-deficient (Bid(-/-)), Bid transgenic mice expressing a nonphosphorable form of Bid and Fas receptor-deficient lpr mice. Apoptosis sensitivity was determined in healthy mice and in mice following bile duct ligation, partial hepatectomy, or suramin pretreatment. As previously reported, loss of Bid protects mice against Jo2-induced liver failure. Remarkably however, Bid(-/-) mice are highly sensitive to MegaFasL-induced apoptosis. MegaFasL-treated Bid(-/-) mice showed a typical type I cell signaling behavior with activation of caspase-3 without Bax translocation to the mitochondria and no cytochrome C/Smac release into the cytosol. In contrast to previous in vitro findings, phosphorylation of Bid does not affect the sensitivity of hepatocytes to Fas receptor-mediated apoptosis in vivo.
conclusionOur data suggest that Bid mainly amplifies a weak death receptor signal in quiescent and nonquiescent hepatocytes rendering the liver more sensitive to FasL-induced apoptosis. Thus, depending on the efficacy of Fas receptor activation, hepatocytes and nonparenchymal cells can either behave as type I or type II cells.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.