ArticleWorld journal of gastroenterology2014
CYLD deletion triggers nuclear factor-κB-signaling and increases cell death resistance in murine hepatocytes.
Article in World journal of gastroenterology, 2014. 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, 16 citations in OpenAlex.
- YTHDC2 Retards Cell Proliferation and Triggers Apoptosis in Papillary Thyroid Cancer by Regulating CYLD-Mediated Inactivation of Akt Signaling.Applied biochemistry and biotechnology · 2024Article
- Inactivation of Tumor Suppressor CYLD Inhibits Fibroblast Reprogramming to Pluripotency.Cancers · 2023Article
- Mitochondria, mitophagy, and the role of deubiquitinases as novel therapeutic targets in liver pathology.Journal of cellular biochemistry · 2022Review
- Hepatocyte Bcl-3 protects from death-receptor mediated apoptosis and subsequent acute liver failure.Cell death & disease · 2022Article
- The Functional Role of Long Non-Coding RNAs in Melanoma.Cancers · 2021Review
- MicroRNAs as the critical regulators of cisplatin resistance in gastric tumor cells.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 2021Review
- The long noncoding RNA CRAL reverses cisplatin resistance via the miR-505/CYLD/AKT axis in human gastric cancer cells.RNA biology · 2020Review
- [Research progress of deubiquitinating enzyme CYLD to regulate liver-related diseases].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2019Review
- lncRNA-MEG3 Suppresses the Proliferation and Invasion of Melanoma by Regulating CYLD Expression Mediated by Sponging miR-499-5p.BioMed research international · 2018Article
- CYLD Deubiquitinase Negatively Regulates High Glucose-Induced NF-BioMed research international · 2017Article
- CYLD downregulates Livin and synergistically improves gemcitabine chemosensitivity and decreases migratory/invasive potential in bladder cancer: the effect is autophagy-associated.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimTo analyze the role of CYLD for receptor-mediated cell death of murine hepatocytes in acute liver injury models.
methodsHepatocyte cell death in CYLD knockout mice (CYLD(-/-) ) was analyzed by application of liver injury models for CD95- (Jo2) and tumor necrosis factor (TNF)-α- [D-GalN/lipopolysaccharide (LPS)] induced apoptosis. Liver injury was assessed by measurement of serum transaminases and histological analysis. Apoptosis induction was quantified by cleaved PARP staining and Western blotting of activated caspases. Nuclear factor (NF)-κB, ERK, Akt and jun amino-terminal kinases signaling were assessed. Primary Hepatocytes were isolated by two step-collagenase perfusion and treated with recombinant TNF-α and with the CD95-ligand Jo2. Cell viability was analyzed by MTT-assay.
resultsLivers of CYLD(-/-) mice showed increased anti-apoptotic NF-κB signaling. In both applied liver injury models CYLD(-/-) mice showed a significantly reduced apoptosis sensitivity. After D-GalN/LPS treatment CYLD(-/-) mice exhibited significantly lower levels of alanine aminotransferase (ALT) (295 U/L vs 859 U/L, P < 0.05) and aspartate aminotransferase (AST) (560 U/L vs 1025 U/L, P < 0.01). After Jo injection CYLD(-/-) mice showed 2-fold lower ALT (50 U/L vs 110 U/L, P < 0.01) and lower AST (250 U/L vs 435 U/L, P < 0.01) serum-levels compared to WT mice. In addition, isolated CYLD(-/-) primary murine hepatocytes (PMH) were less sensitive towards death receptor-mediated apoptosis and showed increased levels of Bcl-2, XIAP, cIAP1/2, survivin and c-FLIP expression upon TNF- and CD95-receptor triggering, respectively. Inhibition of NF-κB activation by the inhibitor of NF-κB phosphorylation inhibitor BAY 11-7085 inhibited the expression of anti-apoptotic proteins and re-sensitized CYLD(-/-) PMH towards TNF- and CD95-receptor mediated cell death.
conclusionCYLD is a central regulator of apoptotic cell death in murine hepatocytes by controlling NF-κB dependent anti-apoptotic signaling.
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