http://purl.uniprot.org/citations/37261903 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/37261903 | http://www.w3.org/2000/01/rdf-schema#comment | "ObjectiveWe aimed to evaluate the association between interleukin (IL)-32 and necroptosis in cholestatic liver injury.MethodsLevels 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.ResultsIn 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.ConclusionIL-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/37261903 | http://purl.org/dc/terms/identifier | "doi:10.1111/1751-2980.13196"xsd:string |
http://purl.uniprot.org/citations/37261903 | http://purl.uniprot.org/core/author | "Fu L."xsd:string |
http://purl.uniprot.org/citations/37261903 | http://purl.uniprot.org/core/author | "Zhao N."xsd:string |
http://purl.uniprot.org/citations/37261903 | http://purl.uniprot.org/core/author | "Zhang X.X."xsd:string |
http://purl.uniprot.org/citations/37261903 | http://purl.uniprot.org/core/author | "Chai J."xsd:string |
http://purl.uniprot.org/citations/37261903 | http://purl.uniprot.org/core/author | "Mao X.R."xsd:string |
http://purl.uniprot.org/citations/37261903 | http://purl.uniprot.org/core/author | "Xu Z.Q."xsd:string |
http://purl.uniprot.org/citations/37261903 | http://purl.uniprot.org/core/author | "Peng S.F."xsd:string |
http://purl.uniprot.org/citations/37261903 | http://purl.uniprot.org/core/date | "2023"xsd:gYear |
http://purl.uniprot.org/citations/37261903 | http://purl.uniprot.org/core/name | "J Dig Dis"xsd:string |
http://purl.uniprot.org/citations/37261903 | http://purl.uniprot.org/core/pages | "293-304"xsd:string |
http://purl.uniprot.org/citations/37261903 | http://purl.uniprot.org/core/title | "Hepatic interleukin 32 attenuates liver injury through repression of necroptosis in cholestasis."xsd:string |
http://purl.uniprot.org/citations/37261903 | http://purl.uniprot.org/core/volume | "24"xsd:string |
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