Inhibition of LPS-induced NO and PGE2 production by asiatic acid via NF-κB inactivation in RAW 264.7 macrophages: Possible involvement of the IKK and MAPK pathways

Yun, Kyung-Jin; Kim, Jiyeon; Kim, Jongbin; Lee, Kyung-Won; Jeong, Seo Young; Park, Hee-Juhn; Jung, Hyun‐Ju; Cho, Young-Wuk; Yun, Kijoo; Lee, Kyung‐Tae

doi:10.1016/j.intimp.2007.11.003

Cited by 238 publications

(147 citation statements)

References 49 publications

(52 reference statements)

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“…NF-κB is a transcription factor that controls a number of genes, such as, iNOS and COX-2, TNF-α, and IL-6, which are important for immunity and inflammation (Barnes et al, 1997;Yun et al, 2008). Upon stimulation with LPS, NF-κB is translocated in the cytoplasm as an inactive complex bound to IκB-α, which is phosphorylated and subsequently degraded, and then dissociates to produce activated NF-κB.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of LPS-induced cyclooxygenase 2 and nitric oxide production by transduced PEP-1-PTEN fusion protein in Raw 264.7 macrophage cells

Lee

Kim

et al. 2008

Exp Mol Med

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Phosphatase and tensin homologue deleted on chromosome 10 (PTEN) is a tumor suppressor. Although it is well known to have various physiological roles in cancer, its inhibitory effect on inflammation remains poorly understood. In the present study, a human PTEN gene was fused with PEP-1 peptide in a bacterial expression vector to produce a genetic in-frame PEP-1-PTEN fusion protein. The expressed and purified PEP-1-PTEN fusion protein were transduced efficiently into macrophage Raw 264.7 cells in a time-and dose-dependent manner when added exogenously in culture media. Once inside the cells, the transduced PEP-1-PTEN protein was stable for 24 h. Transduced PEP-1-PTEN fusion protein inhibited the LPS-induced cyclooxygenase 2 (COX-2) and iNOS expression levels in a dose-dependent manner. Furthermore, transduced PEP-1-PTEN fusion protein inhibited the activation of NF-κB induced by LPS. These results suggest that the PEP-1-PTEN fusion protein can be used in protein therapy for inflammatory disorders.

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Section: Discussionmentioning

confidence: 99%

Inhibition of LPS-induced cyclooxygenase 2 and nitric oxide production by transduced PEP-1-PTEN fusion protein in Raw 264.7 macrophage cells

Lee

Kim

et al. 2008

Exp Mol Med

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“…NF-kB is a transcription factor that controls a number of genes that are important for immunity and inflammation (36,37). LPS stimulation of macrophages activates NF-kB as well as several intracellular signaling pathways, including three MAPK pathways: ERK1/2, p38, and SAPK/JNK.…”

Section: Effect Of Tat-anx1 On Lps-induced Nf-kb and Mapk Activation mentioning

confidence: 99%

Transduced Tat-Annexin protein suppresses inflammation-associated gene expression in lipopolysaccharide (LPS)-stimulated Raw 264.7 cells

Lee

Kim²,

Back³

et al. 2011

BMB Reports

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“…NF-κB activation results from pro-inflammatory stimuli, which coincide with IκB phosphorylation and degradation via the IKK signalosome complex. This process results in the release of free NF-κB dimers (p50 and p65) that translocate to the nucleus where they are involved in the transcription of target genes such as iNOS, TNF-α, and IL-1β [4] . The p38 MAPK signaling pathway plays an important role in promoting inflammatory disease [27] .…”

Section: P<001 (B)mentioning

confidence: 99%

“…Activation of p38 induces the production of key inflammatory mediators. In particular, p38 is activated by LPS stimulation and has been postulated to play an important role in the control of iNOS expression [4] . We have shown that the p38 kinase pathway is an important mediator of NO production by YCP in two ways.…”

Section: P<001 (B)mentioning

confidence: 99%

“…These inflammatory mediators can be both produced and utilized by macrophages in an autocrine fashion. When activated, macrophages can release cytokines, such as IL-1 and NO, to defend against microbial infection and lyse tumor cells [4] . Although the membrane receptor for YCP is not known, some membrane proteins are assumed to act as receptors in macrophages.…”

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confidence: 99%

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Macrophage receptors of polysaccharide isolated from a marine filamentous fungus Phoma herbarum YS4108

et al. 2009

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Aim: YCP, a novel (1,4)-α-D-glucan, was isolated from the mycelium of the marine filamentous fungus Phoma herbarum YS4108. In this work, we investigated a YCP-binding cellular receptor expressed by macrophages and the intracellular signal transduction pathways involved in YCP-induced macrophage activation. Methods: Fluorescence-labeled YCP (fl-YCP) was prepared using the CDAP-activation method. Fluorescence confocal laser microscopy and fluorescence-activated cell sorting (FACS) were used to analyze the effect of fl-YCP on macrophages. To characterize the properties of the YCP receptor, carbohydrates and antibodies were used to inhibit the binding of fl-YCP to macrophages. Moreover, we investigated the role of membrane receptors Toll-like receptor 2 (TLR2), Toll-like receptor 4 (TLR4), Toll-like receptor 6 (TLR6) and complement receptor 3 (CR3). We also examined the role of the p38 kinase pathway in mediating nitric oxide (NO) production. Results: YCP had an in vitro stimulatory effect on the release of NO in macrophage, and fl-YCP can bind directly to receptors on the surface of macrophages in a time-and dose-dependent manner. Competition studies show that LPS, laminarin, anti-TLR4 antibody and anti-CD11b (CR3) antibody could inhibit fl-YCP binding to macrophages. Conversely, mannose, anti-TLR2 and anti-TLR6 antibody could not. Treatment of RAW264.7 cells with YCP resulted in significant activation of p38 in a time-dependent manner. The specific p38 inhibitor SB203580 abrogated YCP-induced NO generation. Treatment of RAW264.7 cells with anti-TLR4 antibody and anti-CR3 antibody significantly reduced YCP-induced NO production and p38 activation. Conclusion: We have demonstrated that YCP-induced NO production occurs through the TLR4 and CR3 membrane receptors in a p38 kinase-dependent manner in macrophages.Keywords: YCP; Phoma herbarum; macrophages; nitric oxide; receptor; p38 kinase Acta Pharmacologica Sinica (2009Sinica ( ) 30: 1008Sinica ( -1014 doi: 10.1038/aps.2009 Original Article Introduction YCP is a polysaccharide with a mean molecular weight of 2.4×10 3 kDa purified from the mycelium of Phoma herbarum YS4108, a marine filamentous fungus that inhabits the sediment at a depth of 50 m in the Yellow Sea near Sheyang Port, Yancheng, China. (YCP is the acronym of Yancheng and polysaccharide.) In an earlier study, YCP was found to be able to increase phagocytic activity of mice in vitro and in vivo, indicating that it may activate macrophages [1] . YCP could significantly increase the production of NO and interleukin-1 (IL-1) by macrophages. It also significantly increased phagocytic activity of macrophages [2] . However, the YCP-binding cellular receptor expressed by macrophages and the intracellular signal transduction pathways involved in YCP-induced macrophage activation are poorly understood.β-glucans are potent stimulators of the innate immune system in invertebrates, while in mammals they are potent activators of the complement system. Soluble and particulate β-glucans interact with cognate receptors on...

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Inhibition of LPS-induced NO and PGE2 production by asiatic acid via NF-κB inactivation in RAW 264.7 macrophages: Possible involvement of the IKK and MAPK pathways

Cited by 238 publications

References 49 publications

Inhibition of LPS-induced cyclooxygenase 2 and nitric oxide production by transduced PEP-1-PTEN fusion protein in Raw 264.7 macrophage cells

Inhibition of LPS-induced cyclooxygenase 2 and nitric oxide production by transduced PEP-1-PTEN fusion protein in Raw 264.7 macrophage cells

Transduced Tat-Annexin protein suppresses inflammation-associated gene expression in lipopolysaccharide (LPS)-stimulated Raw 264.7 cells

Macrophage receptors of polysaccharide isolated from a marine filamentous fungus Phoma herbarum YS4108

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