Activation of c-Jun N-terminal kinase by Akabane virus is required for apoptosis

Mitomo, S; Omatsu, Tsutomu; Tsuchiaka, Shinobu; Nagai, Masashi; Furuya, Tetsuya; Mizutani, Tetsuya

doi:10.1016/j.rvsc.2016.06.007

Cited by 11 publications

(8 citation statements)

References 44 publications

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“…Inhibitor concentrations were selected based on literature, IC50 values, and previous own studies. The concentrations of AER-37 (anti-FcεRIα-Ab; eBioscience, San Diego, CA, USA), c48/80 (Sigma, Steinheim, Germany), and SP (Bachem, Budendorf, Switzerland) were as follows: 0.1 µg/mL, 10 µg/mL, and 30 µM, respectively, in accordance with our previous studies [ 27 , 32 , 54 , 114 , 115 , 116 , 117 ].…”

Section: Methodssupporting

confidence: 57%

Cytokines Stimulated by IL-33 in Human Skin Mast Cells: Involvement of NF-κB and p38 at Distinct Levels and Potent Co-Operation with FcεRI and MRGPRX2

Franke

Wang

Zuberbier

et al. 2021

IJMS

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The IL-1 family cytokine IL-33 activates and re-shapes mast cells (MCs), but whether and by what mechanisms it elicits cytokines in MCs from human skin remains poorly understood. The current study found that IL-33 activates CCL1, CCL2, IL-5, IL-8, IL-13, and TNF-α, while IL-1β, IL-6, IL-31, and VEGFA remain unaffected in cutaneous MCs, highlighting that each MC subset responds to IL-33 with a unique cytokine profile. Mechanistically, IL-33 induced the rapid (1–2 min) and durable (2 h) phosphorylation of p38, whereas the phosphorylation of JNK was weaker and more transient. Moreover, the NF-κB pathway was potently activated, as revealed by IκB degradation, increased nuclear abundance of p50/p65, and vigorous phosphorylation of p65. The activation of NF-κB occurred independently of p38 or JNK. The induced transcription of the cytokines selected for further study (CCL1, CCL2, IL-8, TNF-α) was abolished by interference with NF-κB, while p38/JNK had only some cytokine-selective effects. Surprisingly, at the level of the secreted protein products, p38 was nearly as effective as NF-κB for all entities, suggesting post-transcriptional involvement. IL-33 did not only instruct skin MCs to produce selected cytokines, but it also efficiently co-operated with the allergic and pseudo-allergic/neurogenic activation networks in the production of IL-8, TNF-α, CCL1, and CCL2. Synergism was more pronounced at the protein than at the mRNA level and appeared stronger for MRGPRX2 ligands than for FcεRI. Our results underscore the pro-inflammatory nature of an acute IL-33 stimulus and imply that especially in combination with allergens or MRGPRX2 agonists, IL-33 will efficiently amplify skin inflammation and thereby aggravate inflammatory dermatoses.

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Section: Methodssupporting

confidence: 57%

Cytokines Stimulated by IL-33 in Human Skin Mast Cells: Involvement of NF-κB and p38 at Distinct Levels and Potent Co-Operation with FcεRI and MRGPRX2

Franke

Wang

Zuberbier

et al. 2021

IJMS

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“…Generally speaking, when ZEA induces endoplasmic reticulum stress in renal cells, the expression of CHOP protein increases resulting in the inhibition of the expression of downstream protein Bcl-2, which promotes apoptosis [ 46 , 47 ]. However, when cells are stimulated by the outside world, the protein JNK in the cytoplasm is transformed into p-JNK and phosphorylated and enters the nucleus to promote the expression of apoptotic protein Bax [ 48 , 49 ]. Caspase-12 has no activity when the cells are in normal state.…”

Section: Discussionmentioning

confidence: 99%

Selenium Protects against Zearalenone-Induced Oxidative Stress and Apoptosis in the Mouse Kidney by Inhibiting Endoplasmic Reticulum Stress

Zhang

Wang

et al. 2020

Oxidative Medicine and Cellular Longevity

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This study assessed the molecular mechanism of selenium (Se) protecting against kidney injury induced by zearalenone (ZEA) in mice. The experimental mice were divided into 4 groups including the control group, the Se group, the ZEA group, and the Se+ZEA group; ZEA and Se were administered orally for 28 days. The changes in renal biochemical index (BUN, UA, and CRE), biochemical change of kidney damage such as BUN, UA, and CRE, and oxidative damage such as MDA, T-SOD, and GSH-Px were investigated. Pathological sections and TUNEL staining were used to analyze renal pathological changes and cell apoptosis. qRT-PCR and Western blot were employed to detect the expression of genes and proteins which were related with endoplasmic reticulum stress. The results showed that ZEA increased the concentration of BUN, UA, and CRE and the content of MDA and decreased the activities of T-SOD and GSH-Px in the mouse kidneys. However, Se reversed above changes of the biochemical and antioxidant indexes of renal injury. Moreover, the results also showed that ZEA can increase the expression of Bax, caspase-12, caspase-3, Bip, CHOP, JNK protein, and mRNA and decrease the expression of Bcl-2 protein and mRNA. But Se reversed these proteins and genes related to endoplasmic reticulum stress and apoptosis. It can be concluded that Se protected against the kidney damage induced by ZEA. Se may protect the kidney from ZEA-induced apoptosis and oxidative stress by inhibiting ERS.

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“…ERS can make three kinds of transmembrane signal proteins (IRE1, PERK, and GRP78) dissociate from the chaperone protein GRP78 on the endoplasmic reticulum membrane. These activated receptor proteins can activate the unfolded protein response (UPR) to protect the cells; however, long-term ERS will lead to the activation of the apoptotic proteins CHOP, JNK, and caspase-12 and promote apoptosis of the cells [ 54 , 55 , 56 , 57 ]. Our results showed ZEA can induce ERS, as it promoted the expression of mRNA and protein of the ER resident chaperone GRP78, the most important ERS marker [ 18 ].…”

Section: Discussionmentioning

confidence: 99%

“…The JNK protein is mainly cytoplasmic. JNK converts to its phosphorylated form p-JNK and enters the nucleus to exert its activity when cells are stimulated, resulting in nuclear activation of the transcription factor (c-Jun) [ 61 ] and finally activating Bax and other pro-apoptotic proteins [ 54 ]. Caspase-12 exists in the form of a caspase enzyme (procaspase-12) that is not bioactive when the cells are in a normal state.…”

Section: Discussionmentioning

confidence: 99%

Proanthocyanidins Protect Epithelial Cells from Zearalenone-Induced Apoptosis via Inhibition of Endoplasmic Reticulum Stress-Induced Apoptosis Pathways in Mouse Small Intestines

et al. 2018

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This study evaluated the protective effect of proanthocyanidins (PCs) on reducing apoptosis in the mouse intestinal epithelial cell model MODE-K exposed to zearalenone (ZEA) through inhibition of the endoplasmic reticulum stress (ERS)-induced apoptosis pathway. Our results showed that PCs could reduce the rate of apoptosis in MODE-K cells exposed to ZEA (p < 0.01). PCs significantly increased the ZEA-induced antioxidant protective effects on the enzymes superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) and on the content of GSH. PCs also significantly decreased the ZEA-induced increase in the content of malondialdehyde (MDA). The analysis indicated that ZEA increased both mRNA and protein expression levels of C/EBP homologous protein (CHOP), GRP78, c-Jun N-terminal kinase (JNK), and cysteinyl aspartate specific proteinase 12 (caspase-12) (p < 0.05), which are related to the ERS-induced apoptosis pathway. ZEA decreased levels of the pro-apoptotic related protein Bcl-2 (p < 0.05) and increased the anti-apoptotic related protein Bax (p < 0.05). Co-treatment with PCs was also shown to significantly reverse the expression levels of these proteins in MODE-K cells. The results demonstrated that PCs could protect MODE-K cells from oxidative stress and apoptosis induced by ZEA. The underlying mechanism may be that PCs can alleviate apoptosis in mouse intestinal epithelial cells by inhibition of the ERS-induced apoptosis pathway.

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Activation of c-Jun N-terminal kinase by Akabane virus is required for apoptosis

Cited by 11 publications

References 44 publications

Cytokines Stimulated by IL-33 in Human Skin Mast Cells: Involvement of NF-κB and p38 at Distinct Levels and Potent Co-Operation with FcεRI and MRGPRX2

Cytokines Stimulated by IL-33 in Human Skin Mast Cells: Involvement of NF-κB and p38 at Distinct Levels and Potent Co-Operation with FcεRI and MRGPRX2

Selenium Protects against Zearalenone-Induced Oxidative Stress and Apoptosis in the Mouse Kidney by Inhibiting Endoplasmic Reticulum Stress

Proanthocyanidins Protect Epithelial Cells from Zearalenone-Induced Apoptosis via Inhibition of Endoplasmic Reticulum Stress-Induced Apoptosis Pathways in Mouse Small Intestines

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