Interleukin-35 Regulates Angiogenesis Through P38 Mitogen-Activated Protein Kinase Signaling Pathway in Interleukin-1β-Stimulated SW1353 Cells and Cartilage Bioinformatics Analysis

Yang, Jie; Yao, Lutian; Li, Yuxuan; Gao, Ruoxi; Huo, Ran; Xia, Liping; Shen, Hui; Lu, Jin‐Jian

doi:10.1089/jir.2021.0016

Cited by 2 publications

(2 citation statements)

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“…In this study, the effect of IL-35 on p38 protein expression in TNF-α-induced cells was detected by Western blot. The results again verified that IL-35 could inhibit the high expression of p38 protein, which is consistent with the findings in previous studies [ 10 , 26 ]. Subsequently, to further verify that IL-35 inhibited inflammatory response, cell pyroptosis and cell injury via p38 MAPK signaling pathway in TNF-α-induced BEAS-2B cells, P79350 was added to the experimental group as a p38 agonist.…”

Section: Discussionsupporting

confidence: 92%

“…To further investigate the mechanism of IL-35 action on cell pyroptosis in TNF-α-induced BEAS-2B cells, the p38 MAPK signaling pathway was introduced in this study. The study revealed that IL-35 could regulate IL-1beta-stimulated angiogenesis in SW1353 cells and cartilage through the p38 MAPK signaling pathway [ 26 ]. And other study proved that IL-35 could increase the sensitivity of monocytes in asthma patients to glucocorticoid treatment by regulating p38 MAPK [ 10 ].…”

Section: Discussionmentioning

confidence: 99%

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IL-35 inhibits cell pyroptosis and attenuates cell injury in TNF-α-induced bronchial epithelial cells via p38 MAPK signaling pathway

et al. 2022

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Asthma is a chronic inflammatory disease of the airways, and IL-35 has been found to be involved in the pathogenesis of inflammatory diseases by mediating the inhibition of effector T cells. But the role of IL-35 on cell pyroptosis, which frequently occurs in inflammatory diseases, has not been elucidated. Therefore, the present study used a TNF-α-induced bronchial epithelial cell injury model to investigate the mechanism of IL-35 action on cell pyroptosis and asthma injury. The effects of IL-35 on cell activity, inflammatory factor levels, cell barrier damage and cell pyroptosis-related proteins were examined by CCK-8, ELISA, lucifer yellow permeability and Western blotting assay, respectively. Subsequently, following the activation of p38 MAPK signaling pathway by adding p38 agonist, the effect of IL-35 on TNF-α-induced bronchial epithelial cell injury was investigated. The results showed that IL-35 reduced TNF-α-induced cell injury, decreased inflammatory factors, improved cell permeability, and inhibited cell pyroptosis. More importantly, the effect of IL-35 on injured cells was reversed after p38 MAPK pathway was activated. In summary, IL-35 inhibited p38 MAPK pathway to suppress cell pyroptosis and thereby reduce asthma injury.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 99%