Silica induces nuclear factor-κB activation through TAK1 and NIK in Rat2 cell line

Cho, HyeYoung; Lee, JooYong; Kwak, Noh-Jin; Lee, Kweon-Haeng; Rha, SukJoo; Kim, Young-Hoon; Cho, Yong-Yeun; Yang, Ki-Hwa; Kim, Kyoung Ah; Lim, Yejee

doi:10.1016/s0378-4274(03)00193-0

Cited by 11 publications

(6 citation statements)

References 26 publications

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“…Diesel exhaust particle exposure, much like exposure to CS, induces an increase of lung neutrophils, macrophages, and T-lymphocytes in experimental animals (19) and has recently been shown to increase COPD mortality in railroad workers (11). Similarly, silica exposure, which has also been associated with the development of COPD (7), was shown to activate the NF-B pathway in a TAK1-dependent manner in lung fibroblasts (6). Collectively, these and our data indicate that TAK1 may be linked to inflammatory responses induced by environmental stimuli on various cell types that have been implicated in the development of COPD.…”

Section: Discussionmentioning

confidence: 99%

Role for TAK1 in cigarette smoke-induced proinflammatory signaling and IL-8 release by human airway smooth muscle cells

Pera

Atmaj

Vegt

et al. 2012

American Journal of Physiology-Lung Cellular and Molecular Phys

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Chronic obstructive pulmonary disease (COPD) is an inflammatory disease, characterized by a progressive decline in lung function. Airway smooth muscle (ASM) mass may be increased in COPD, contributing to airflow limitation and proinflammatory cytokine production. Cigarette smoke (CS), the major risk factor of COPD, causes ASM cell proliferation, as well as interleukin-8 (IL-8)-induced neutrophilia. In various cell types, transforming growth factor-β-activated kinase 1 (TAK1) plays a crucial role in MAP kinase and NF-κB activation, as well as IL-8 release induced by IL-1β, TNF-α, and lipopolysaccharide. The role of TAK1 in CS-induced IL-8 release is not known. The aim of this study was to investigate the role of TAK1 in CS-induced NF-κB and MAP kinase signaling and IL-8 release by human ASM cells. Stimulation of these cells with CS extract (CSE) increased IL-8 release and ERK-1/2 phosphorylation, as well as Iκ-Bα degradation and p65 NF-κB subunit phosphorylation. CSE-induced ERK-1/2 phosphorylation and Iκ-Bα degradation were both inhibited by pretreatment with the specific TAK1 inhibitor LL-Z-1640-2 (5Z-7-oxozeaenol; 100 nM). Similarly, expression of dominant-negative TAK1 inhibited CSE-induced ERK-1/2 phosphorylation. In addition, inhibitors of TAK1 and the NF-κB (SC-514; 50 μM) and ERK-1/2 (U-0126; 3 μM) signaling inhibited the CSE-induced IL-8 release by ASM cells. These data indicate that TAK1 plays a major role in CSE-induced ERK-1/2 and NF-κB signaling and in IL-8 release by human ASM cells. Furthermore, they identify TAK1 as a novel target for the inhibition of CS-induced inflammatory responses involved in the development and progression of COPD.

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Section: Discussionmentioning

confidence: 99%

Role for TAK1 in cigarette smoke-induced proinflammatory signaling and IL-8 release by human airway smooth muscle cells

Pera

Atmaj

Vegt

et al. 2012

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…Some studies report that exposure to diesel exhaust particles, PM 2.5 , and silica induced activation of NF-B in vitro and in vivo (Cho et al, 2003;Hirota et al, 2008;Shukla et al, 2000).…”

Section: Discussionmentioning

confidence: 99%

Expression of cytokine-induced neutrophil chemoattractant in rat lungs by intratracheal instillation of nickel oxide nanoparticles

Nishi

Morimoto

Ogami

et al. 2009

Inhalation Toxicology

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Since nanoparticles easily agglomerate to form larger particles, it is important to maintain the size of their agglomerates at the nano-level to evaluate the harmful effect of the nanoparticles. We prevented agglomeration of nickel oxide nanoparticles by ultrasound diffusion and filtration, established an acute exposure model using animals, and examined inflammation and chemokine expression. The mass median diameter of nickel oxide nanoparticle agglomerates suspended in distilled water for intratracheal instillation was 26 nm (8.41 nm weighted average surface primary diameter). Male Wistar rats received intratracheal instillation of nickel oxide nanoparticles at 0.1 mg (0.33 mg/kg) or 0.2 mg (0.66 mg/kg), and were dissected 3 days, 1 week, 1 month, 3 months, and 6 months after the instillation. The control group received intratracheal instillation of distilled water. Three chemokines (cytokine-induced neutrophil chemoattractant-1 (CINC-1), CINC-2alphabeta, and CINC-3) in the lung tissue and bronchoalveolar lavage fluid (BALF) were determined by quantitative measurement of protein by ELISA. Both CINC-1 and CINC-2alphabeta concentration was elevated from day 3 to 3 months in lung tissue and from day 3 to 6 months in BALF. On the other hand, CINC-3 was elevated on day 3 in both lung tissue and BALF, and then decreased. The total cell and neutrophil counts in BALF were increased from day 3 to 3 months. In lung tissue, infiltration of mainly neutrophils and alveolar macrophages was observed from day 3 to 6 months in alveoli. These results suggest that CINC was involved in lung injury by nickel oxide nanoparticles.

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“…In vitro, it was reported that activation of AP-1 is induced through reactive oxygen species generated by crystalline silica in JB6 cells 15) . Cho et al 16) have reported that silica induces NF-κB activation through TAK1 and NIK in the Rat2 cell line. Moreover, experimental animal models indicate that activation of NF-κB is associated with silica-induced pulmonary inflammation and the inhibition of its activation corresponds with suppression of inflammation 17) .…”

Section: Discussionmentioning

confidence: 99%

Expression of Heme Oxygenase‐1 in the Lungs of Rats Exposed to Crystalline Silica

Nagatomo

Morimoto

Oyabu

et al. 2006

Journal of Occupational Health

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Expression of Heme Oxygenase-1 in the Lungs of Rats Exposed to Crystalline Silica: Hiroko NAGATOMO, et al. Department of Occupational Pneumology, Institute of Industrial and Ecological Sciences, University of Occupational and Environmental Health-Oxidative stress is thought to be the pathogenesis of pulmonary fibrosis induced by particles, and heme oxygenase-1 (HO-1) protects lung tissue against oxidative stress. We hypothesized that HO-1 is also associated with oxidative lung injury caused by exposure to particles. The present study was conducted to investigate the time course of HO-1 expression of lungs exposed to crystalline silica in vivo. Male Wistar rats were administered 1 mg or 2 mg of crystalline silica suspended in saline by a single intratracheal instillation and were sacrificed at 3 d, 1 wk, 1 month, 3 months and 6 months of recovery time. The expression of HO-1 was observed by western blot analysis and immunostaining. Protein levels of HO-1 were increased compared to the controls at 3 d, and from 1 month to 6 months following intratracheal instillation of 2 mg of crystalline silica. The levels of HO-1 were increased compared to the controls from 1 month to 6 months following intratracheal instillation of 1 mg of crystalline silica. Many HO-1 positive cells were found particularly in the alveolar macrophages during immunostaining. These findings suggest that HO-1 is related to lung injury arising from exposure to crystalline silica. (J Occup Health 2006; 48: 124-128)

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Silica induces nuclear factor-κB activation through TAK1 and NIK in Rat2 cell line

Cited by 11 publications

References 26 publications

Role for TAK1 in cigarette smoke-induced proinflammatory signaling and IL-8 release by human airway smooth muscle cells

Role for TAK1 in cigarette smoke-induced proinflammatory signaling and IL-8 release by human airway smooth muscle cells

Expression of cytokine-induced neutrophil chemoattractant in rat lungs by intratracheal instillation of nickel oxide nanoparticles

Expression of Heme Oxygenase‐1 in the Lungs of Rats Exposed to Crystalline Silica

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