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Interleukin-13 promotes cellular senescence through inducing mitochondrial dysfunction in IgG4-related sialadenitis

International Journal of Oral Science 2022年第3期14卷 321-333页

作者： Mengqi Zhu Sainan Min xiangdi mao Yuan Zhou Yan Zhang Wei Li Li Li Liling Wu Xin Cong Guangyan Yu Department of Oral and Maxillofacial Surgery Peking University School and Hospital of Stomatology&National Center of Stomatology&National Clinical Research Center for Oral Diseases&National Engineering Research Center of Oral Biomaterials and Digital Medical DevicesBeijingChina Department of Physiology and Pathophysiology Peking University School of Basic Medical SciencesKey Laboratory of Molecular Cardiovascular SciencesMinistry of Educationand Beijing Key Laboratory of Cardiovascular Receptors ResearchBeijingChina Department of Biomedical Informatics Peking University School of Basic Medical SciencesKey Laboratory of Molecular Cardiovascular SciencesMinistry of EducationBeijingChina

Immunoglobulin G4-related sialadenitis(IgG4-RS)is an immune-mediated fibro-inflammatory disease and the pathogenesis is still not fully *** aim of this study was to explore the role and mechanism of interleukin-13(IL-13)in the cellular senescence during the progress of *** found that the expression of IL-13 and IL-13 receptorα1(IL-13Rα1)as well as the number of senescent cells were significantly higher in the submandibular glands(SMGs)of IgG4-RS ***-13 directly induced senescence as shown by the elevated activity of senescence-associatedβ-galactosidase(SA-β-gal),the decreased cell proliferation,and the upregulation of senescence markers(p53 and p16)and senescence-associated secretory phenotype(SASP)factors(IL-1βand IL-6)in SMG-C6 ***,IL-13 increased the level of phosphorylated signal transducer and activator of transcription 6(p-STAT6)and mitochondrial-reactive oxygen species(mt ROS),while decreased the mitochondrial membrane potential,ATP level,and the expression and activity of superoxide dismutase 2(SOD2).Notably,the IL-13-induced cellular senescence and mitochondrial dysfunction could be inhibited by pretreatment with either STAT6 inhibitor AS1517499 or mitochondria-targeted ROS scavenger Mito ***,IL-13 increased the interaction between p-STAT6 and c AMP-response element binding protein(CREB)-binding protein(CBP)and decreased the transcriptional activity of CREB on *** together,our findings revealed a critical role of IL-13 in the induction of salivary gland epithelial cell senescence through the elevated mitochondrial oxidative stress in a STAT6–CREB–SOD2-dependent pathway in IgG4-RS.

关键词： Interleukin-13 promotes cellular senescence through inducing mitochondrial dysfunction in IgG4-related sialadenitis IgG

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