Protein kinase C stimulates human B cell activating factor gene expression through reactive oxygen species-dependent c-Fos in THP-1 pro-monocytic cells

Lee, Geunhee; Lee, Mi-Hee; Yoon, Yeo-Dae; Kang, Jong Soon; Pyo, Suhkneung; Moon, Eun‐Yi

doi:10.1016/j.cyto.2012.03.017

Cited by 9 publications

(10 citation statements)

References 42 publications

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“…Suppression of the signal pathway by specific inhibitors was additionally shown to induce inhibition of signal molecules in the previous studies (Chen et al, 2010;Wiejak et al, 2012;Zang et al, 2010). As an inhibitor, SP suppressed the production of PKC, which was in line with the former studies (Kim, Chang, & Jung, 2012;Lee et al, 2012). PKC plays an important part in the initial events of signal transduction, which is crucial to the activation of T lymphocytes (Giacomo et al, 2010).…”

Section: Discussionsupporting

confidence: 77%

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Involvement of the PKC–NF–κB signaling pathway in the regulation of T lymphocytes proliferation of chickens by conjugated linoleic acids

Long

Yang

Liú

et al. 2015

Food and Agricultural Immunology

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The involvement of protein kinase C (PKC) and nuclear factor-κB (NF-κB) signaling pathway in immunoregulatory actions of conjugated linoleic acid (CLA) in chicken T lymphocyte was investigated. T lymphocytes in peripheral blood were isolated and cultured. The PKC and NF-κB inhibitors, staurosporine (SP) and pyrrolidine dithiocarbamate (PDTC), were used. SP inhibited the production of PKC, and PDTC partly blocked the NF-κB mRNA relative expression. Data suggested compared with c9, t11-CLA and t10, c12-CLA groups, the attenuated effects were showed in SP or PDTC treatment with the application of CLA, which suggested PKC and NF-κB mediated in the immunity of CLA. Furthermore, SP and PDTC inhibited the IL-2 secretion and T lymphocyte proliferation. SP or PDTC induced reduction of IL-2 secretion and T-lymphocytes proliferation were greatly or partially attenuated by CLA isomers. In conclusion, CLA was a potent immunomodulator for T lymphocytes through targeting the PKC-NF-κB pathway.

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Section: Discussionsupporting

confidence: 77%

“…Note: a,b,c,d Means in the same row without the same superscript differ significantly (P < 0.05). (Kim et al, 2012;Lee et al, 2012;Ling, Yang, Tan, Chui, & Chew, 2010), our data revealed that at least under the condition of SP stimulation, PKC production was decreased, thus implicating the involvement of PKC in T lymphocyte proliferation.…”

Section: Discussionmentioning

confidence: 50%

Involvement of the PKC–NF–κB signaling pathway in the regulation of T lymphocytes proliferation of chickens by conjugated linoleic acids

Long

Yang

Liú

et al. 2015

Food and Agricultural Immunology

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“…Given that hBAFF promoter construct ranges from 0.25 to 1.0 kb, 32 we examined where HIF-1 α affects the hBAFF promoter. As shown in Figure 5a, when MH7A cells were transfected with different sizes of hBAFF promoter plasmids, hBAFF promoter activity increased significantly after treatment with TNF- α .…”

Section: Resultsmentioning

confidence: 99%

“…Luciferase units of experimental vector were normalized to the control vector in each sample. 31, 32, 48 …”

Section: Methodsmentioning

confidence: 99%

Synovial cell death is regulated by TNF-α-induced expression of B-cell activating factor through an ERK-dependent increase in hypoxia-inducible factor-1α

Lee

et al. 2017

Cell Death Dis

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B-cell activating factor (BAFF) has a role in the maturation and maintenance of B cells and is associated with rheumatoid arthritis (RA). Here, we investigated whether tumor necrosis factor (TNF)-α-induced BAFF expression controls the survival of fibroblast-like synoviocytes (FLS) and whether their survival can be regulated by TNF-α-mediated upregulation of hypoxia-inducible factor (HIF)-1α using MH7A synovial cells transfected with the SV40 T antigen. More TNF-α-treated cells died compared with the control. Survival was increased by incubation with Z-VAD but inhibited after transfection with BAFF-siRNA. Both BAFF and HIF-1α expression were enhanced when MH7A cells were treated with TNF-α. TNF-α-induced BAFF expression decreased in response to HIF-1α-siRNA, whereas it increased under hypoxia or by overexpressing HIF-1α. The HIF-1α binding site on the BAFF promoter (−693 to −688 bp) was confirmed by chromatin immunoprecipitation assay to detect the −750 to −501 bp and −800 to −601 bp regions. The BAFF promoter increased in response to TNF-α treatment or overexpression of HIF-1α. However, TNF-α-induced BAFF expression and promoter activity decreased after treatment with the ERK inhibitor PD98059. Cell death was enhanced by PD98059 but was inhibited by overexpression of HIF-1α. Taken together, our results demonstrate that BAFF expression to control synovial cell survival was regulated by HIF-1α binding to the BAFF promoter, and suggest for the first time that HIF-1α might be involved in the production of inflammatory cytokines to regulate the physiological function of rheumatic FLS.

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“…ROS are usually implicated in cellular inflammatory responses. PMA activates protein kinase C (PKC) and leads to ROS production [35]. ROS increase oxidative stress, activate the NFKB and MAPK signaling pathways, and promote the production of inflammatory factors such as IL1, IL6, and TNFa [36], which in turn increase ROS [37].…”

Section: Discussionmentioning

confidence: 99%

miR-181a Regulates Inflammation Responses in Monocytes and Macrophages

et al. 2013

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miR-181a has been presumed to target the 3′-untranslated regions (3′-UTR) of IL1a based on software predictions. miR-181a and IL1a have opposite expression levels in monocytes and macrophages in the inflammatory state. This led us to suspect that mir-181a has an important function in regulating inflammatory response by targeting IL1a. Fluorescence reporter assays showed that miR-181a effectively binds to the 3′-UTR of IL1a. The anti-inflammatory functions of miR-181a were investigated in lipopolysaccharides (LPS)-induced Raw264.7 and phorbol 12-myristate 13-acetate (PMA)/LPS-induced THP-1 cells. We found that miR-181a mimics significantly lowered IL1a expression levels in these cells and, interestingly, miR-181a inhibitors reversed this decrease. In addition, miR-181a mimics significantly inhibited increase in the levels of inflammatory factors (IL1b, IL6, and TNFa) in these cells. Furthermore, miR-181a mimics and inhibitors decreased and increased, respectively, production of reactive oxygen species in PMA/LPS-induced THP-1 cells. These results indicate that miR-181a regulates inflammatory responses by directly targeting the 3′-UTR of IL1a and down-regulating IL1a levels. Interestingly, we found that miR-181a inhibited production of inflammatory factors even in IL1a-induced THP-1 cells, suggesting that the anti-inflammatory effects of miR-181a possibly involves other targets in addition to IL1a. Thus, we provide the first evidence for anti-inflammatory effects of miR-181a mediated at least in part by down-regulating IL1a.

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Protein kinase C stimulates human B cell activating factor gene expression through reactive oxygen species-dependent c-Fos in THP-1 pro-monocytic cells

Cited by 9 publications

References 42 publications

Involvement of the PKC–NF–κB signaling pathway in the regulation of T lymphocytes proliferation of chickens by conjugated linoleic acids

Involvement of the PKC–NF–κB signaling pathway in the regulation of T lymphocytes proliferation of chickens by conjugated linoleic acids

Synovial cell death is regulated by TNF-α-induced expression of B-cell activating factor through an ERK-dependent increase in hypoxia-inducible factor-1α

miR-181a Regulates Inflammation Responses in Monocytes and Macrophages

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