Role of transcriptional factors Sp1, c-Rel, and c-Jun in LPS-induced C/EBPδ gene expression of mouse macrophages

Liu, Yiwen; Chen, C. C.; Wang, Ju‐Ming; Chang, Wen-Chang; Huang, Yung-Chieh; Chung, Seung-Tae; Chen, Ben‐Kuen; Hung, Jan Jong

doi:10.1007/s00018-007-7375-5

Cited by 27 publications

(29 citation statements)

References 49 publications

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“…Previous studies mention C/EBPd regulation and conclude that NF-kB, Erk1/2, and c-Jun recruitment by Sp1 are important [Liu et al, 2007]. In this study, we found that there is no obvious alteration in the activation of NF-kB and Erk1/2 in LPS-treated cells after TSA treatment (Supplementary Fig.…”

Section: Discussionsupporting

confidence: 35%

“…Moreover, COX-2 accumulation has been detected in different tumor types [Dempke et al, 2001;Gately and Kerbel, 2003;Toomey et al, 2009]. Previous studies have indicated that LPS can induce COX-2 expression via activation of NF-kB and upregulation of C/EBPs [Woo et al, 2006;Liu et al, 2007]. Herein, we also found that COX-2 could be induced, and in parallel, NF-kB Fig.…”

Section: Discussionmentioning

confidence: 51%

“…4b). Furthermore, as in previous studies, c-Jun could be induced and recruited to the promoter through the Sp1 after LPS treatment [Liu et al, 2007], but interestingly, c-Jun could not be recruited via Sp1 to the promoter of C/EBPd after LPS-treated cells were treated with TSA (Fig. 4c).…”

Section: Tsa Represses the Recruitment Of C-jun By Sp1 To The Promotementioning

confidence: 60%

“…Previous studies have revealed that NF-kB activation leads to IkB degradation, c-Rel and Rel A nuclear accumulation, and ERK1/2 phosphorylation after LPS treatment of RAW264.7 cells [Liu et al, 2007]. In this study, we first checked the c-Rel and Rel A levels in the nuclear extract to detect the activation of the NF-kB pathway after TSA and LPS treatments ( Supplementary Fig.…”

Section: No Significant Difference In the Lps-induced Activation Of Nmentioning

confidence: 99%

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Inhibition of LPS‐induced C/EBPδ by trichostatin a has a positive effect on LPS‐induced cyclooxygenase 2 expression in RAW264.7 cells

Liu

Wang

Hsu

et al. 2010

J of Cellular Biochemistry

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Cyclooxygenase 2 (COX-2) is an important inflammatory factor. Previous studies have indicated that COX-2 is induced with lipopolysaccharide (LPS) treatment. Here, we found that an inhibitor of histone deacetylase (HDAC), trichostatin A (TSA), cannot repress LPS-induced COX-2 but it increased the COX-2 level in RAW264.7 cells. We found no significant difference in NF-kappaB activation and ERK1/2 phosphorylation, but LPS-induced C/EBP delta expression was completely abolished after TSA treatment of LPS-treated cells. Interesting, reporter assay of C/EBP delta promoter revealed that Sp1-binding site is important. Although there was no alteration in c-Jun levels, but the phosphorylation of c-Jun at its C-terminus was increased dramatically. A DNA-associated protein assay (DAPA) and chromatin immunoprecipitation assay (ChIP) indicated that c-Jun was recruited via Sp1 to the promoter of C/EBP delta after LPS treatment; this recruitment of c-Jun was repressed by TSA. C/EBP delta inhibition by TSA resulted in increased binding of C/EBP alpha and C/EBP beta to the COX-2 promoter. Therefore, TSA has a positive effect on LPS-induced COX-2 since it decreases the C/EBP delta level by reducing c-Jun recruitment by Sp1 to the C/EBP delta promoter, resulting in increased the recruitment of C/EBP alpha and C/EBP beta to the COX-2 promoter.

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Section: Discussionsupporting

confidence: 35%

Section: Discussionmentioning

confidence: 51%

Section: Tsa Represses the Recruitment Of C-jun By Sp1 To The Promotementioning

confidence: 60%

Section: No Significant Difference In the Lps-induced Activation Of Nmentioning

confidence: 99%

See 2 more Smart Citations

Inhibition of LPS‐induced C/EBPδ by trichostatin a has a positive effect on LPS‐induced cyclooxygenase 2 expression in RAW264.7 cells

Liu

Wang

Hsu

et al. 2010

J of Cellular Biochemistry

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“…15,16 A previous report indicated that expression of some C/EBP family member may be regulated by MAPKs and NF-B. 17 To examine possible involvement of MAPKs or NF-B in the induction of C/EBP␤ by ER stress, we pretreated mesangial cells with selective inhibitors of extracellular signal-regulated kinase (PD098059), JNK (SP600125), p38 MAPK (SB203580), or NF-B (SC-514); stimulated them by thapsigargin; and subjected them to Northern blot analysis. Our preliminary results showed that SP600125 but not other inhibitors attenuated induction of C/EBP␤ by ER stress (Supplemental Figure S3), indicating possible involvement of JNK.…”

Section: Discussionmentioning

confidence: 98%

ER Stress Depresses NF-κB Activation in Mesangial Cells through Preferential Induction of C/EBPβ

Hayakawa

Nakajima

Hiramatsu

et al. 2010

Journal of the American Society of Nephrology

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Modest induction of endoplasmic reticulum (ER) stress confers resistance to inflammation in glomeruli. Recently, we found that ER stress leads to mesangial insensitivity to cytokine-induced activation of NF-B, but the underlying mechanisms are incompletely understood. ER stress can trigger expression of CCAAT/enhancer-binding proteins (C/EBPs), which interact with transcription factors including NF-B. Here, we investigated a role for C/EBPs in the ER stress-induced resistance to cytokines. Mesangial cells preferentially induced C/EBP␤ after exposure to thapsigargin or tunicamycin; induction of C/EBP␦ was modest and transient, and expression of C/EBP␣ was absent. The induction of C/EBP␤ correlated with accumulation of C/EBP␤ protein and enhanced transcriptional activity of C/EBP. Overexpression of C/EBP␤ markedly suppressed TNF-␣-induced activation of NF-B, independent of its transacting potential. Knockdown of C/EBP␤ by small interfering RNA reversed the suppressive effect of ER stress on NF-B. In vivo, preconditioning of mice with ER stress induced renal C/EBP␤ and suppressed NF-Bdependent gene expression in response to LPS. Using dominant negative mutants and null mutants for individual branches of the unfolded protein response, we identified the RNA-dependent protein kinaselike ER kinase (PERK) and the inositol-requiring ER-to-nucleus signal kinase 1 (IRE1) pathways as the unfolded protein response responsible for ER stress-induced C/EBP␤. These results suggest that ER stress blunts cytokine-triggered activation of NF-B, in part through PERK-and IRE1-mediated preferential induction of C/EBP␤.

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Artemisinic acid is a regulator of adipocyte differentiation and C/EBP δ expression

Lee

Kim

Lee

et al. 2012

J of Cellular Biochemistry

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Adipocyte dysfunction is associated with the development of obesity. In this study, artemisinic acid, which was isolated from Artemisia annua L., inhibited adipogenic differentiation of human adipose tissue-derived mesenchymal stem cells (hAMSCs) and its mechanism of action was determined. The mRNA levels of peroxidase proliferation-activated receptor (PPAR) γ and CCAAT/enhancer binding protein (C/EBP) α, late adipogenic factors, were reduced by artemisinic acid. Moreover, the mRNA levels of the PPAR γ target genes lipoprotein lipase, CD36, adipocyte protein, and liver X receptor were down-regulated by artemisinic acid. Artemisinic acid reduced expression of the C/EBP δ gene without impacting C/EBP β. In addition, attempts to elucidate a possible mechanism underlying the artemisinic acid-mediated effects revealed that reduced expression of the C/EBP δ gene was mediated by inhibiting Jun N-terminal kinase (JNK). Additionally, artemisinic acid also reduced the expression of the adipogenesis-associated genes glucose transporter-4 and vascular endothelial growth factor. In addition to the interference of artemisinic acid with adipogenesis, artemisinic acid significantly attenuated tumor necrosis factor-α-induced secretion of interleukin-6 by undifferentiated hAMSCs, thus influencing insulin resistance and the inflammatory state characterizing obesity. Taken together, these findings indicate that inhibiting adipogenic differentiation of hAMSCs by artemisinic acid occurs primarily through reduced expression of C/EBP δ, which is mediated by the inhibition of JNK and suggest that aremisinic acid may be used as a complementary treatment option for obesity associated with metabolic syndrome.

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Role of transcriptional factors Sp1, c-Rel, and c-Jun in LPS-induced C/EBPδ gene expression of mouse macrophages

Cited by 27 publications

References 49 publications

Inhibition of LPS‐induced C/EBPδ by trichostatin a has a positive effect on LPS‐induced cyclooxygenase 2 expression in RAW264.7 cells

Inhibition of LPS‐induced C/EBPδ by trichostatin a has a positive effect on LPS‐induced cyclooxygenase 2 expression in RAW264.7 cells

ER Stress Depresses NF-κB Activation in Mesangial Cells through Preferential Induction of C/EBPβ

Artemisinic acid is a regulator of adipocyte differentiation and C/EBP δ expression

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