Selective modulation of lipopolysaccharide-stimulated cytokine expression and mitogen-activated protein kinase pathways by dibutyryl-cAMP in BV2 microglial cells

Woo, Moon Sook; Jang, Pil Geum; Park, Jin-Sun; Kim, Won Ki; Joh, Tong H.; Kim, Hee Sun

doi:10.1016/s0169-328x(03)00095-0

Cited by 70 publications

(77 citation statements)

References 51 publications

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“…This second messenger has been reported to inhibit certain proinflammatory pathways such as the LPS-induced p38 and JNK pathways (32)(33)(34). However, in this study we show that AM/AMBP-1 also induces PPAR-␥ expression in LPS stimulated macrophages in vitro and in vivo.…”

Section: Discussioncontrasting

confidence: 66%

Vasoactive Hormone Adrenomedullin and Its Binding Protein: Anti-Inflammatory Effects by Up-Regulating Peroxisome Proliferator-Activated Receptor-γ

Miksa

Cui

et al. 2007

The Journal of Immunology

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Sepsis is a critical inflammatory condition from which numerous patients die due to multiple organ failure and septic shock. The vasoactive hormone adrenomedullin (AM) and its binding protein (AMBP-1) are beneficial in sepsis by abrogating the progression to irreversible shock and decreasing proinflammatory cytokine release. To investigate the anti-inflammatory mechanism, we studied to determine the effect of the AM/AMBP-1 complex on peroxisome proliferator-activated receptor-γ (PPAR-γ) expression and activation by using RAW264.7 cells and a rat endotoxemia model. LPS treatment significantly decreased PPAR-γ expression in vivo and in vitro and was associated with increased TNF-α production. Treatment with AM/AMBP-1 for 4 h completely restored PPAR-γ levels in both models, resulting in TNF-α suppression. In a knockdown model using small interfering RNA in RAW264.7 macrophages, AM/AMBP-1 failed to suppress TNF-α production in the absence of PPAR-γ. LPS caused the suppression of intracellular cyclic AMP (cAMP), which was prevented by simultaneous AM/AMBP-1 treatment. Although incubation with dibutyryl cAMP significantly decreased LPS-induced ΤΝF-α release, it did not alter PPAR-γ expression. Through inhibition studies using genistein and PD98059 we found that the Pyk-2 tyrosine kinase-ERK1/2 pathway is in part responsible for the AM/AMBP-1-mediated induction of PPAR-γ and the anti-inflammatory effect. We conclude that AM/AMBP-1 is protective in sepsis due to its vasoactive properties and direct anti-inflammatory effects mediated through both the cAMP-dependent pathway and Pyk-2-ERK1/2-dependent induction of PPAR-γ.

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Section: Discussioncontrasting

confidence: 66%

Vasoactive Hormone Adrenomedullin and Its Binding Protein: Anti-Inflammatory Effects by Up-Regulating Peroxisome Proliferator-Activated Receptor-γ

Miksa

Cui

et al. 2007

The Journal of Immunology

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“…Nuclear extracts from treated microglia were prepared as previously described (27). Double-stranded DNA oligonucleotides containing the NF-kB or AP-1 consensus sequences (Promega) were end-labeled using T4 polynucleotide kinase (NEB, Beverly, MA) in the presence of [g-32 P]ATP.…”

Section: Emsasmentioning

confidence: 99%

“…Double-stranded DNA oligonucleotides containing the NF-kB or AP-1 consensus sequences (Promega) were end-labeled using T4 polynucleotide kinase (NEB, Beverly, MA) in the presence of [g-32 P]ATP. One microgram of nuclear proteins were incubated with 32 P-labeled NF-kB or AP-1 probe on ice for 30 min and resolved on 5% acrylamide gels, as previously described (27). For supershift assays, Abs against the p65 or p50 subunits of NF-kB (Santa Cruz Biotechnology) were coincubated with nuclear extract mixes for 30 min at 4˚C before adding the radiolabeled probe.…”

Section: Emsasmentioning

confidence: 99%

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α-Synuclein Activates Microglia by Inducing the Expressions of Matrix Metalloproteinases and the Subsequent Activation of Protease-Activated Receptor-1

Lee

Woo

Moon

et al. 2010

The Journal of Immunology

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243

191

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“…Specific inhibitors of p38 MAPK have been proven to reduce inflammation, slow down microglia activation and provide neuroprotective effects [15,[30][31][32]. Recently, studies have shown that compounds that inhibit p38 MAPK activation in microglia represent potential anti-inflammatory effects and protect neurons against excitotoxicity or LPS-induced neurotoxicity [9,20,33].…”

Section: Discussionmentioning

confidence: 99%

Protective effect of 1,2,4-benzenetriol on LPS-induced NO production by BV2 microglial cells

Hou

Chen

et al. 2005

J Biomed Sci

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SummaryHydroxyhydroquinone or 1,2,4-benzenetriol (BT) detected in the beverages has a structure that coincides with the water-soluble form of a sesame lignan, sesamol. We previously showed that sesame antioxidants had neuroprotective abilities due to their antioxidant properties and/or inducible nitric oxide synthase (iNOS) inhibition. However, studies show that BT can induce DNA damage through the generation of reactive oxygen species (ROS). Therefore, we were interested to investigate the neuroprotective effect of BT in vitro and in vivo. The results showed that instead of enhancing free radical generation, BT dosedependently (10-100 lM) attenuated nitrite production, iNOS mRNA and protein expression in lipopolysaccharide (LPS)-stimulated murine BV-2 microglia. BT significantly reduced LPS-induced NF-jB and p38 MAPK activation. It also significantly reduced the generation of ROS in H 2 O 2 -induced BV-2 cells and in H 2 O 2 -cellfree conditions. The neuroprotective effect of BT was further demonstrated in the focal cerebral ischemia model of Sprague-Dawley rat. Taken together, the inhibition of LPS-induced nitrite production might be due to the suppression of NF-jB, p38 MAPK signal pathway and the ROS scavenging effect. These effects might help to protect neurons from the ischemic injury.

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Selective modulation of lipopolysaccharide-stimulated cytokine expression and mitogen-activated protein kinase pathways by dibutyryl-cAMP in BV2 microglial cells

Cited by 70 publications

References 51 publications

Vasoactive Hormone Adrenomedullin and Its Binding Protein: Anti-Inflammatory Effects by Up-Regulating Peroxisome Proliferator-Activated Receptor-γ

Vasoactive Hormone Adrenomedullin and Its Binding Protein: Anti-Inflammatory Effects by Up-Regulating Peroxisome Proliferator-Activated Receptor-γ

α-Synuclein Activates Microglia by Inducing the Expressions of Matrix Metalloproteinases and the Subsequent Activation of Protease-Activated Receptor-1

Protective effect of 1,2,4-benzenetriol on LPS-induced NO production by BV2 microglial cells

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