ArticleGastroenterology2006
Sustained phosphorylation of Bid is a marker for resistance to Fas-induced apoptosis during chronic liver diseases.
Article in Gastroenterology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 31 citations in OpenAlex.
- Apoptotic cell death in disease-Current understanding of the NCCD 2023.Cell death and differentiation · 2023Review
- InGene expression · 2018Article
- Senescence and cell death in chronic liver injury: roles and mechanisms underlying hepatocarcinogenesis.Oncotarget · 2018Review
- Cordycepin induces apoptosis in human liver cancer HepG2 cells through extrinsic and intrinsic signaling pathways.Oncology letters · 2016Article
- Proliferative versus apoptotic functions of caspase-8 Hetero or homo: the caspase-8 dimer controls cell fate.Biochimica et biophysica acta · 2012Review
- Protection from rapamycin-induced apoptosis by insulin-like growth factor-I is partially dependent on protein kinase C signaling.Cancer research · 2010Article
- The strength of the Fas ligand signal determines whether hepatocytes act as type 1 or type 2 cells in murine livers.Hepatology (Baltimore, Md.) · 2009Article
- Death by committee: organellar trafficking and communication in apoptosis.Traffic (Copenhagen, Denmark) · 2009Review
- Targeting cancer cells by ROS-mediated mechanisms: a radical therapeutic approach?Nature reviews. Drug discovery · 2009Review
- At the crossroads of homoeostasis and disease: roles of the PACS proteins in membrane traffic and apoptosis.The Biochemical journal · 2009Review
- Principles of therapeutic liver repopulation.Journal of inherited metabolic diseaseReview
Corrections and comments
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Authors and funding
8 authors at 5 institutions in 3 countries.
Funding
Abstract
BACKGROUND &
aimsIncreased rates of apoptosis have been reported to play a role in the pathophysiology of many disorders, including liver diseases. Conversely, genetic mutations that result in impairment of programmed cell death have been associated with cancer development. However, apoptosis resistance can also be the result of nongenetic stress adaptation, as seen in the cancer-prone metabolic liver disease hereditary tyrosinemia. To clarify whether stress-induced apoptosis resistance is a general feature of chronic liver diseases, an animal model of chronic cholestasis was examined.
methodsStudies were performed with mice before and 2 weeks following bile duct ligation and with Fah-/- and Fah/p21-/- mice before and after NTBC withdrawal.
resultsHere we show that bile duct ligation induced profound resistance against Fas monoclonal antibody-mediated hepatocyte death. The apoptosis signaling pathway was blocked downstream of caspase-8 activation and proximal to mitochondrial cytochrome c release. In controls, activation of the Fas receptor resulted in rapid dephosphorylation of Bid and its subsequent cleavage, whereas Bid remained phosphorylated and uncleaved in chronic cholestasis and other models of hepatic apoptosis resistance.
conclusionsWe propose a model in which the phosphorylation status of Bid determines the apoptotic threshold of hepatocytes in vivo. Furthermore, resistance to apoptosis in chronic cholestasis may contribute to the long-term risk of cancer in this setting.
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