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http://purl.uniprot.org/citations/37261903http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/37261903http://www.w3.org/2000/01/rdf-schema#comment"

Objective

We aimed to evaluate the association between interleukin (IL)-32 and necroptosis in cholestatic liver injury.

Methods

Levels of necroptosis-related markers in cholestatic and control patients, including the receptor-interacting serine-threonine kinase 3 (RIPK3), receptor-interacting serine-threonine kinase 1 (RIPK1), and mixed lineage kinase domain-like (MLKL) were measured. Animal experiments in C57BL/6J and transgenic mice with IL32β/γ overexpression were also conducted to confirm the effect of IL-32 on necroptosis in cholestasis, which was induced by α-naphthylisothiocyanate (ANIT) and 1% lithocholic acid (LCA). PLC/PRF/5-ASBT and primary mouse hepatocytes were utilized for the investigation of the regulation and mechanism of IL-32 in cholestasis.

Results

In the liver tissues of cholestatic patients, the mRNA and protein expressions of RIPK1, RIPK3, and MLKL were increased and associated with IL-32 expression. In addition, expressions of these indicators in the liver of 1% LCA- and ANIT-induced mouse models were significantly increased, while they were markedly decreased in hIL32βLTg and hIL32γLTg mice. After bile acid stimulation, IL-32 and phosphorylated Akt (p-Akt) expressions significantly elevated in a dose-dependent manner. After treated with tumor necrosis factor (TNF)-α, IL-32 inhibited MLKL expression in primary mouse hepatocytes.

Conclusion

IL-32 is negatively associated with necroptosis in cholestatic patients. Moreover, IL-32 is induced by p-Akt and effectively attenuates necroptosis in ANIT- or 1% LCA-induced cholestasis."xsd:string
http://purl.uniprot.org/citations/37261903http://purl.org/dc/terms/identifier"doi:10.1111/1751-2980.13196"xsd:string
http://purl.uniprot.org/citations/37261903http://purl.uniprot.org/core/author"Fu L."xsd:string
http://purl.uniprot.org/citations/37261903http://purl.uniprot.org/core/author"Zhao N."xsd:string
http://purl.uniprot.org/citations/37261903http://purl.uniprot.org/core/author"Zhang X.X."xsd:string
http://purl.uniprot.org/citations/37261903http://purl.uniprot.org/core/author"Chai J."xsd:string
http://purl.uniprot.org/citations/37261903http://purl.uniprot.org/core/author"Mao X.R."xsd:string
http://purl.uniprot.org/citations/37261903http://purl.uniprot.org/core/author"Xu Z.Q."xsd:string
http://purl.uniprot.org/citations/37261903http://purl.uniprot.org/core/author"Peng S.F."xsd:string
http://purl.uniprot.org/citations/37261903http://purl.uniprot.org/core/date"2023"xsd:gYear
http://purl.uniprot.org/citations/37261903http://purl.uniprot.org/core/name"J Dig Dis"xsd:string
http://purl.uniprot.org/citations/37261903http://purl.uniprot.org/core/pages"293-304"xsd:string
http://purl.uniprot.org/citations/37261903http://purl.uniprot.org/core/title"Hepatic interleukin 32 attenuates liver injury through repression of necroptosis in cholestasis."xsd:string
http://purl.uniprot.org/citations/37261903http://purl.uniprot.org/core/volume"24"xsd:string
http://purl.uniprot.org/citations/37261903http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/37261903
http://purl.uniprot.org/citations/37261903http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/37261903
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http://purl.uniprot.org/uniprot/#_G3LU47-mappedCitation-37261903http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/37261903
http://purl.uniprot.org/uniprot/#_P24001-mappedCitation-37261903http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/37261903
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