ATF-2 regulates lipopolysaccharide-induced transcription in macrophage cells

Hirose, Noriyuki; Maekawa, Tomoko; Shinagawa, Toshie; Ishii, Shunsuke

doi:10.1016/j.bbrc.2009.05.001

Cited by 33 publications

(21 citation statements)

References 23 publications

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“…This finding is underscored by the fact that RAW264.7 macrophages responded to LPS by enhanced ATF-2 and ATF-3 expression in the present investigation. These observations appear to be in line with those reported by other investigators as well [44,45].…”

Section: Tegdma-induced Activation Of Transcription Factors Related Tsupporting

confidence: 94%

“…As a target of JNK/p38 signaling, phosphorylation of ATF-2 was increased in RAW264.7 macrophages after stimulation with lipopolysaccharide (LPS). Consequently, it was suggested that ATF-2 might be involved in the transcriptional control mediated by Toll-like receptors (TLRs) in mouse macrophages [44]. We have recently shown that LPS-stimulated cytokine production was instantaneously downregulated in the presence of TEGDMA [17].…”

Section: Tegdma-induced Activation Of Transcription Factors Related Tmentioning

confidence: 98%

See 1 more Smart Citation

Activation of stress-regulated transcription factors by triethylene glycol dimethacrylate monomer

Krifka¹,

Petzel²,

Bolay³

et al. 2011

Biomaterials

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Section: Tegdma-induced Activation Of Transcription Factors Related Tsupporting

confidence: 94%

Section: Tegdma-induced Activation Of Transcription Factors Related Tmentioning

confidence: 98%

Activation of stress-regulated transcription factors by triethylene glycol dimethacrylate monomer

Krifka¹,

Petzel²,

Bolay³

et al. 2011

Biomaterials

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“…When treated with TSA prior to LPS stimulation, SOCS3 expression was inhibited. These results indicate that HDAC1 positively regulates AFT2 expression, and thereby positively regulates the expression of SOCS3 [ 120 ].…”

Section: Negative Regulation Of Jak/stat Pathway By Socs Proteinsmentioning

confidence: 69%

Regulation of the Jak/STATs Pathways by Histone Deacetylases

Woods

Lienlaf-Moreno

Sotomayor

et al. 2013

Nuclear Signaling Pathways and Targeting Transcription in Cancer

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The regulation of the Jak/STAT pathways involves multiple mechanisms, some of them exclusive to individual cascades, and other shared amongst them. Additionally, there is increasing evidence to support the interconnection of these cascades with other intracellular signaling pathways, which are regulated by independent factors. Thus, the understanding of the Jak/STAT pathway regulation is still growing and recently being revisited to account for the participation of nonconventional regulators. Acetylation of proteins is an emerging regulatory mechanism with demonstrated involvement in the regulation of several intracellular pathways. Specifi cally, the participation of histone deacetylases (HDACs) is garnering attention due to the feasibility of inhibition of their activity and the subsequent control over the cellular processes being modulated by them. This chapter 156 will explore and present the current knowledge about the role of HDACs and their inhibitors in the control of members of the Jak/STAT pathways and direct activators/modulators of their signaling.

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“…5D). The marker of JNK activation, ATF2, is also a target of p38 signaling in inflammatory cells (Brown et al, 2008;Hirose et al, 2009), but as shown in Fig. 5E, SB203580 did not reduce phosphorylation of ATF2, arguing for ATF2 as a selective target for JNK in this model.…”

Section: Discussionmentioning

confidence: 81%

Trovafloxacin Potentiation of Lipopolysaccharide-Induced Tumor Necrosis Factor Release from RAW 264.7 Cells Requires Extracellular Signal-Regulated Kinase and c-Jun N-Terminal Kinase

Poulsen

Albee

Ganey

et al. 2014

J Pharmacol Exp Ther

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Trovafloxacin (TVX) is a fluoroquinolone antibiotic known to cause idiosyncratic, drug-induced liver injury (IDILI) in humans. The mechanism underlying this toxicity remains unknown. Previously, an animal model of IDILI in mice revealed that TVX synergizes with inflammatory stress from bacterial lipopolysaccharide (LPS) to produce a hepatotoxic interaction. The liver injury required prolongation of the appearance of tumor necrosis factor-a (TNF) in the plasma. The results presented here describe a model of TVX/LPS coexposure in RAW 264.7 cells acting as a surrogate for TNFreleasing cells in vivo. Pretreating cells with TVX for 2 hours before LPS addition led to increased TNF protein release into culture medium in a concentration-and time-dependent manner relative to cells treated with LPS or TVX alone. During the pretreatment period, TVX increased TNF mRNA, but this was less apparent when cells were exposed to TVX after LPS addition, suggesting that the pivotal signaling events that increase TNF expression occurred during the TVX pretreatment period. Indeed, TVX exposure increased activation of extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), and p38 mitogen-activated protein kinase. Inhibition of either ERK or JNK decreased the TVX-mediated increase in TNF mRNA and LPS-induced TNF protein release, but p38 inhibition did not. These results demonstrated that the increased TNF appearance from TVX-LPS interaction in vivo can be reproduced in vitro and occurs in an ERK-and JNK-dependent manner.

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ATF-2 regulates lipopolysaccharide-induced transcription in macrophage cells

Cited by 33 publications

References 23 publications

Activation of stress-regulated transcription factors by triethylene glycol dimethacrylate monomer

Activation of stress-regulated transcription factors by triethylene glycol dimethacrylate monomer

Regulation of the Jak/STATs Pathways by Histone Deacetylases

Trovafloxacin Potentiation of Lipopolysaccharide-Induced Tumor Necrosis Factor Release from RAW 264.7 Cells Requires Extracellular Signal-Regulated Kinase and c-Jun N-Terminal Kinase

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