Components of diesel exhaust particles differentially affect lung expression of cyclooxygenase‐2 related to bacterial endotoxin

Inoue, Ken‐ichiro; Takano, Hirohisa; Yanagisawa, Rie; Ichinose, Takamichi; Sadakane, Kaori; Yoshino, Shigefumi; Yamaki, Kouya; Uchiyama, Kazuhiko; Yoshikawa, Toshikazu

doi:10.1002/jat.984

Cited by 14 publications

(12 citation statements)

References 23 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The current findings are consistent with these prior reports and establish the importance of the NF-B/ COX-2 signaling pathway during RANKL induction in FLS. While it has recently been shown that silica particles induce COX-2 in fibroblasts (8,17,35), the current studies are the first to implicate a calpain-dependent mechanism.…”

Section: Discussionmentioning

confidence: 86%

Titanium particles stimulate COX-2 expression in synovial fibroblasts through an oxidative stress-induced, calpain-dependent, NF-κB pathway

Wei¹,

Flick²,

Drissi³

et al. 2009

American Journal of Physiology-Cell Physiology

View full text Add to dashboard Cite

In prosthetic loosening, bone resorption is induced by wear debris particles generated from the artificial joint articulation. Our prior work showed that synovial-like fibroblasts respond to titanium particles by producing receptor activator of NF-kappaB ligand (RANKL), a critical activator of osteoclastogenesis. While this effect occurs through a cyclooxygenase-2 (COX-2)-dependent pathway, the mechanism of COX-2 stimulation by titanium particles is not clear. Here we show that titanium particles induce COX-2 gene expression by activating NF-kappaB signaling. Inhibitor of NF-kappaB (IkappaBalpha) is degraded following particle treatment, permitting active NF-kappaB to translocate to the nucleus where it interacts with the COX-2 promoter and drives transcription. NF-kappaB activation is dependent on reactive oxygen species since antioxidants block the NF-kappaB signaling induced by particles. Surprisingly, IkappaBalpha degradation is independent of IKK (IkappaB kinase) and the 26S proteasome. Instead, calpain inhibitor can block the IkappaBalpha degradation induced by particles. Furthermore, the calpain-targeted COOH-terminal PEST sequence of IkappaBalpha is necessary for phosphorylation and degradation, consistent with a proteasome-independent mechanism of catabolism. Altogether, the data demonstrate a signaling pathway by which titanium particles induce oxidative stress, stimulate calpain-mediated NF-kappaB activation, and activate target gene expression, including COX-2. These findings define important targets for osteolysis but may also have importance in other diseases where fibroblasts respond to environmental particles, including pulmonary diseases.

show abstract

Section: Discussionmentioning

confidence: 86%

Titanium particles stimulate COX-2 expression in synovial fibroblasts through an oxidative stress-induced, calpain-dependent, NF-κB pathway

Wei¹,

Flick²,

Drissi³

et al. 2009

American Journal of Physiology-Cell Physiology

View full text Add to dashboard Cite

show abstract

“…In order to elucidate which components of the organic DEP fraction was responsible for inflammatory responses, different extracts have been analyzed (i.e., primarily those drawn into methanol [Inoue et al, 1997] or dichloromethane [Inoue et al, 2004]). Other Investigators have used a benzene extract containing about 82% of all the B[a]P in DEP to study its effect on IL-8 secretion by epithelial cells (Kawasaki et al, 2001).…”

Section: Discussionmentioning

confidence: 99%

Effect of Polycyclic Aromatic Hydrocarbons and Carbon Black Particles on Pro-Inflammatory Cytokine Secretion: Impact of PAH Coating Onto Particles

Goulaouic¹,

Foucaud²,

Bennasroune³

et al. 2008

Journal of Immunotoxicology

View full text Add to dashboard Cite

It has been suggested that the organic fraction of particulate matter in air pollution has a major role in the toxicity of this pollutant, notably via its effects on inflammation. The major organic compounds adsorbed onto these particles are polycyclic aromatic hydrocarbons (PAH), among which benzo In general, coating the CB with PAH did not modify the effect of the CB alone; the exception was that LPS-induced IL-1β secretion was reduced. In contrast, ultrafine CB (14 nm diameter: ufCB) caused a decrease in cytokine secretion; this effect was modified by PAH coating. For example, PAH coating on ufCB amplified the inhibitory effect of ufCB against IL-1β secretion but did not modify IL-8 formation. Moreover, PAH coating on ufCB tended to minimize the effect of LPS stimulation; this included (i) inhibition of the decrease in IL-12 secretion induced by uncoated ufCB and (ii) stimulation of IL-10 production. It was concluded that adsorption of PAH onto these particles could decrease their bioavailability and so their abilities to affect cell cytokine production. The results also showed that when PAH were adsorbed onto the fine particles, any observed increases in cytokine secretion consistently appeared to be due to the particles themselves. In contrast, while ufCB alone almost uniformly led to decreases in cytokine formation by the

show abstract

“…Feeding trials were conducted to investigate the effects of 9c,11t-CLA and 10t,12c-CLA isomers on COX-2 protein expression and PGE 2 release in vivo. Mouse lung was selected based on known COX-2 expression and PGE 2 release from this organ after inflammatory stimulation (18,(38)(39)(40). As shown in Fig.…”

Section: Discussionmentioning

confidence: 99%

10t,12c-conjugated linoleic acid inhibits lipopolysaccharide-induced cyclooxygenase expression in vitro and in vivo

Barnes

Bütz

et al. 2005

Journal of Lipid Research

View full text Add to dashboard Cite

Previous data demonstrated that conjugated linoleic acid (CLA) reduced eicosanoid release from select organs. We hypothesized that one active CLA isomer was responsible for the reduced prostaglandin release and that the mechanism was through the inhibition of inducible cyclooxygenase-2 (COX-2). Here, we examined the effects of 10t,12c-CLA and 9c,11t-CLA on COX-2 protein/mRNA expression, prostaglandin E 2 (PGE 2 ) production, and the mechanism by which CLA affects COX-2 expression and prostaglandin release. The COX-2 protein expression level was inhibited 80% by 10t, 12c-CLA and 26% by 9c,11t-CLA at 100 M in vitro. PGE 2 production was decreased from 5.39 to 1.12 ng/2 ؋ 10 6 cells by 10t,12c-CLA and from 5.7 to 4.5 ng/2 ؋ 10 6 cells by 9c,11t-CLA at 100 M. Mice fed 10t,12c-CLA but not 9c,11t-CLA were found to have a 34% decrease in COX-2 protein and a 43% reduction of PGE 2 release in the lung. 10t,12c-CLA reduced COX-2 mRNA expression level by 30% at 100 M in vitro and by 30% in mouse lung in vivo. Reduced COX-2 mRNA was attributable to an inhibition of the nuclear factor B (NF-B) pathway by 10t,12c-CLA. These data suggested that the inhibition of NF-B was one of the mechanisms for the reduced COX-2 expression and PGE 2 release by 10t,12c-

show abstract

Components of diesel exhaust particles differentially affect lung expression of cyclooxygenase‐2 related to bacterial endotoxin

Cited by 14 publications

References 23 publications

Titanium particles stimulate COX-2 expression in synovial fibroblasts through an oxidative stress-induced, calpain-dependent, NF-κB pathway

Titanium particles stimulate COX-2 expression in synovial fibroblasts through an oxidative stress-induced, calpain-dependent, NF-κB pathway

Effect of Polycyclic Aromatic Hydrocarbons and Carbon Black Particles on Pro-Inflammatory Cytokine Secretion: Impact of PAH Coating Onto Particles

10t,12c-conjugated linoleic acid inhibits lipopolysaccharide-induced cyclooxygenase expression in vitro and in vivo

Contact Info

Product

Resources

About