Up‐regulation of heme oxygenase‐1 expression through the Rac1/NADPH oxidase/ROS/p38 signaling cascade mediates the anti‐inflammatory effect of 15‐deoxy‐Δ<sup>12,14</sup>‐prostaglandin J<sub>2</sub> in murine macrophages

Hong, Hyeyoung; Jeon, Woo-Kwang; Kim, Byung-Chul

doi:10.1016/j.febslet.2008.02.012

Cited by 38 publications

(20 citation statements)

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“…Additionally, 15dPGJ 2 is able to activate cytoprotective mechanisms, such as the induction of HO-1 expression, in an NF-κB-independent fashion [30]. Similar results have been described by our group in human lymphocytes [32], and by other researchers in murine macrophages [65]. Therefore, accumulating evidence of 15dPGJ 2 pro-inflammatory actions [22], [23], [66], [67] taken altogether makes its anti-inflammatory properties increasingly controversial [24]–[27], [31].…”

Section: Discussionsupporting

confidence: 83%

Transcription of Liver X Receptor Is Down-Regulated by 15-Deoxy-Δ12,14-Prostaglandin J2 through Oxidative Stress in Human Neutrophils

et al. 2012

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Liver X receptors (LXRs) are ligand-activated transcription factors of the nuclear receptor superfamily. They play important roles in controlling cholesterol homeostasis and as regulators of inflammatory gene expression and innate immunity, by blunting the induction of classical pro-inflammatory genes. However, opposite data have also been reported on the consequences of LXR activation by oxysterols, resulting in the specific production of potent pro-inflammatory cytokines and reactive oxygen species (ROS). The effect of the inflammatory state on the expression of LXRs has not been studied in human cells, and constitutes the main aim of the present work. Our data show that when human neutrophils are triggered with synthetic ligands, the synthesis of LXRα mRNA became activated together with transcription of the LXR target genes ABCA1, ABCG1 and SREBP1c. An inflammatory mediator, 15-deoxy-Δ12,14-prostaglandin J2 (15dPGJ2), hindered T0901317-promoted induction of LXRα mRNA expression together with transcription of its target genes in both neutrophils and human macrophages. This down-regulatory effect was dependent on the release of reactive oxygen species elicited by 15dPGJ2, since it was enhanced by pro-oxidant treatment and reversed by antioxidants, and was also mediated by ERK1/2 activation. Present data also support that the 15dPGJ2-induced serine phosphorylation of the LXRα molecule is mediated by ERK1/2. These results allow to postulate that down-regulation of LXR cellular levels by pro-inflammatory stimuli might be involved in the development of different vascular diseases, such as atherosclerosis.

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Section: Discussionsupporting

confidence: 83%

Transcription of Liver X Receptor Is Down-Regulated by 15-Deoxy-Δ12,14-Prostaglandin J2 through Oxidative Stress in Human Neutrophils

et al. 2012

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“…Our observations showed that only 15Δ-PGJ 2 stimulated L6 cell proliferation while PGF 2 α and PGE 2 were found to be without effect. Evidence supporting the role of 15Δ-PGJ 2 in the resolution phase of inflammation is growing [45-47]; furthermore, it was shown to stimulate human fetal foreskin fibroblast proliferation [22]. In our model, the stimulating effect induced by 15Δ-PGJ 2 was very significant and further underlines the importance of COX-2 activity.…”

Section: Discussionsupporting

confidence: 56%

Mast cell tryptase stimulates myoblast proliferation; a mechanism relying on protease-activated receptor-2 and cyclooxygenase-2

Duchesne

Tremblay

Côté

2011

BMC Musculoskelet Disord

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BackgroundMast cells contribute to tissue repair in fibrous tissues by stimulating proliferation of fibroblasts through the release of tryptase which activates protease-activated receptor-2 (PAR-2). The possibility that a tryptase/PAR-2 signaling pathway exists in skeletal muscle cell has never been investigated. The aim of this study was to evaluate whether tryptase can stimulate myoblast proliferation and determine the downstream cascade.MethodsProliferation of L6 rat skeletal myoblasts stimulated with PAR-2 agonists (tryptase, trypsin and SLIGKV) was assessed. The specificity of the tryptase effect was evaluated with a specific inhibitor, APC-366. Western blot analyses were used to evaluate the expression and functionality of PAR-2 receptor and to assess the expression of COX-2. COX-2 activity was evaluated with a commercial activity assay kit and by measurement of PGF2α production. Proliferation assays were also performed in presence of different prostaglandins (PGs).ResultsTryptase increased L6 myoblast proliferation by 35% above control group and this effect was completely inhibited by APC-366. We confirmed the expression of PAR-2 receptor in vivo in skeletal muscle cells and in satellite cells and in vitro in L6 cells, where PAR-2 was found to be functional. Trypsin and SLIGKV increased L6 cells proliferation by 76% and 26% above control, respectively. COX-2 activity was increased following stimulation with PAR-2 agonist but its expression remained unchanged. Inhibition of COX-2 activity by NS-398 abolished the stimulation of cell proliferation induced by tryptase and trypsin. Finally, 15-deoxy-Δ-12,14-prostaglandin J2 (15Δ-PGJ2), a product of COX-2-derived prostaglandin D2, stimulated myoblast proliferation, but not PGE2 and PGF2α.ConclusionsTaken together, our data show that tryptase can stimulate myoblast proliferation and this effect is part of a signaling cascade dependent on PAR-2 activation and on the downstream activation of COX-2.

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“…NADPH oxidase-ROS-p38 signaling and up-regulation of HO-1 in murine macrophages treated with LPS (36). This pathway differs from ours because, although RAC1 Q61L induced a slight increase in ROS production (Fig.…”

Section: Discussioncontrasting

confidence: 52%

Transcription Factors NRF2 and NF-κB Are Coordinated Effectors of the Rho Family, GTP-binding Protein RAC1 during Inflammation

Cuadrado

Martín‐Moldes

et al. 2014

Journal of Biological Chemistry

261

170

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Background: RAC1 is a small G-protein of the Rho family that activates the transcription factor NF-B to elicit an inflammatory response. Results: We have found that RAC1 also induces the NRF2/ARE pathway, which in term blocks RAC1-dependent NF-B activation. Conclusion: RAC1 modulates inflammation by coordinating the activity of pro-inflammatory NF-B and anti-oxidant NRF2 transcription factors. Significance: Therapeutic intervention on RAC1 could help modulate pro-and anti-inflammatory processes.

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Up‐regulation of heme oxygenase‐1 expression through the Rac1/NADPH oxidase/ROS/p38 signaling cascade mediates the anti‐inflammatory effect of 15‐deoxy‐Δ^12,14‐prostaglandin J₂ in murine macrophages

Cited by 38 publications

References 31 publications

Transcription of Liver X Receptor Is Down-Regulated by 15-Deoxy-Δ12,14-Prostaglandin J2 through Oxidative Stress in Human Neutrophils

Transcription of Liver X Receptor Is Down-Regulated by 15-Deoxy-Δ12,14-Prostaglandin J2 through Oxidative Stress in Human Neutrophils

Mast cell tryptase stimulates myoblast proliferation; a mechanism relying on protease-activated receptor-2 and cyclooxygenase-2

Transcription Factors NRF2 and NF-κB Are Coordinated Effectors of the Rho Family, GTP-binding Protein RAC1 during Inflammation

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Up‐regulation of heme oxygenase‐1 expression through the Rac1/NADPH oxidase/ROS/p38 signaling cascade mediates the anti‐inflammatory effect of 15‐deoxy‐Δ12,14‐prostaglandin J2 in murine macrophages

Cited by 38 publications

References 31 publications

Transcription of Liver X Receptor Is Down-Regulated by 15-Deoxy-Δ12,14-Prostaglandin J2 through Oxidative Stress in Human Neutrophils

Transcription of Liver X Receptor Is Down-Regulated by 15-Deoxy-Δ12,14-Prostaglandin J2 through Oxidative Stress in Human Neutrophils

Mast cell tryptase stimulates myoblast proliferation; a mechanism relying on protease-activated receptor-2 and cyclooxygenase-2

Transcription Factors NRF2 and NF-κB Are Coordinated Effectors of the Rho Family, GTP-binding Protein RAC1 during Inflammation

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Up‐regulation of heme oxygenase‐1 expression through the Rac1/NADPH oxidase/ROS/p38 signaling cascade mediates the anti‐inflammatory effect of 15‐deoxy‐Δ^12,14‐prostaglandin J₂ in murine macrophages