Activation-induced cell death in human peripheral blood lymphocytes after stimulation with silicate in vitro.

Aikoh, T; Tomokuni, A; Matsukii, T; Hyodoh, Fuminori; Ueki, Hiroshi; Otsuki, Takemi; Ueki, Ayako

doi:10.3892/ijo.12.6.1355

Cited by 39 publications

(43 citation statements)

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“…Therefore, there is a possibility that cell cycle arrest (Levresse et al 1997) and apoptosis (Aikoh et al 1998;Broaddus et al 1996;Dopp et al 1995;Hamilton et al 1996;Wu et al 2000) found in cells exposed to chrysotile might be caused by an activated form of p53 protein. On the other hand, in transgenic mice with reduced and enhanced p53 functions specifically targeted within the pulmonary epithelium, asbestos exposure induced less and more severe fibrogenic lesions in the lung, respectively (Nelson et al 2001).…”

Section: Discussionmentioning

confidence: 99%

Phosphorylation of p53 protein in A549 human pulmonary epithelial cells exposed to asbestos fibers.

Matsuoka

Ichikawa

Morimoto

2003

Environ Health Perspect

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We examined effects of asbestos exposure on the phosphorylation of p53 protein in human pulmonary epithelial type II cells (A549), which express wild-type p53. In cells exposed to two different types of asbestos, chrysotile (approximately 1-6% iron content) and crocidolite (approximately 27% iron content) fibers, at the doses of 1, 5, and 10 microg/cm2 for 24 hr, the levels of p53 phosphorylated at Ser15 and p53 protein were correlated with the dose. On a per-weight basis, chrysotile was more potent in inducing Ser15 phosphorylation and accumulation of p53 protein than was crocidolite. After exposure to 10 micro g/cm2 chrysotile, the levels of p53 phosphorylated at Ser15 and of p53 protein increased after 18 hr. Among serines in p53 protein immunoprecipitated from A549 cells treated with chrysotile, only Ser15 was markedly phosphorylated. In contrast, no clear phosphorylation was observed at Ser6, Ser9, Ser20, Ser37, Ser46, or Ser392. Blocking of the extracellular signal-regulated protein kinase pathway with U0126 or inhibition of p38 activity with SB203580 did not suppress chrysotile-induced Ser15 phosphorylation. On the other hand, treatment with wortmannin, an inhibitor of DNA-activated protein kinase and ataxia-telangiectasia mutated, suppressed both chrysotile-induced Ser15 phosphorylation and accumulation of p53 protein. Treatment with either catalase or N-acetylcysteine failed to suppress chrysotile-induced Ser15 phosphorylation, suggesting that reactive oxygen species do not play a major role in the phosphorylation of p53 protein. The present results show that asbestos, particularly chrysotile, induces phosphorylation of p53 protein at Ser15 in A549 cells depending on a DNA damage-signaling pathway.

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Section: Discussionmentioning

confidence: 99%

Phosphorylation of p53 protein in A549 human pulmonary epithelial cells exposed to asbestos fibers.

Matsuoka

Ichikawa

Morimoto

2003

Environ Health Perspect

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“…Smallsized cells, which imply the apoptotic cells, also increased on day 4 of the incubation (Fig. 6-a, 6-b) 21) . The percentage of monocytes contained among PBMC was calculated with an anti-CD14 monoclonal antibody.…”

Section: Fig 5 (A) Flow Cytometrical Quantitation Of Fitc-dutp Incomentioning

confidence: 99%

“…White, chrysotile (-); Black, chrysotile (+) 21) . Superantigens such as staphyococcal enterotoxin B are known to cause activation-induced cell death (a type of apoptosis ) in human T cells 20) .…”

Section: Fig 5 (A) Flow Cytometrical Quantitation Of Fitc-dutp Incomentioning

confidence: 99%

Biological Effects of Asbestos Fibers on Human Cells In Vitro. Especially on Lymphocytes and Neutrophils.

Ueki

2001

INDUSTRIAL HEALTH

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“…We have also found that asbestos polyclonally activated CD4+ T cells and caused activation-induced cell death (67,68). In addition, PBMCs from HD exposed to asbestos in culture underwent apoptosis; however, many patients with asbestosis have had chronic occupational or other recurrent exposures to silicates.…”

Section: Immunological Effects Of Chrysotile Asbestosmentioning

confidence: 86%

Keynote lecture in the 13th Japanese Society of Immunotoxicology (JSIT 2006)

Otsuki

Miura

Maeda

et al. 2007

Environ Health Prev Med

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Silica and silicates may disturb immune functions such as autoimmunity and tumor immunity, because people who are exposed to the materials sometimes develop autoimmune and malignant diseases, respectively. Although silica-induced disorders of autoimmunity have been explained as adjuvant-type effects of silica, more precise analyses are needed and should reflect the recent progress in immunomolecular findings. A brief summary of our investigations related to the immunological effects of silica/asbestos is presented. Recent advances in immunomolecular studies led to detailed analyses of the immunological effects of asbestos and silica. Both affect immuno-competent cells and these effects may be associated with the pathophysiological development of complications in silicosis and asbestos-exposed patients such as the occurrence of autoimmune disorders and malignant tumors, respectively. In addition, immunological analyses may lead to the development of new clinical tools for the modification of the pathophysiological aspects of diseases such as the regulation of autoimmunity or tumor immunity using cell-mediated therapies, various cytokines, and molecule-targeting therapies. In particular, as the incidence of asbestos-related malignancies is increasing and such malignancies have been a medical and social problem since the summer in 2005 in Japan, efforts should be focused on developing a cure for these diseases to eliminate the nation wide anxiety about these malignancies.

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Activation-induced cell death in human peripheral blood lymphocytes after stimulation with silicate in vitro.

Cited by 39 publications

References 0 publications

Phosphorylation of p53 protein in A549 human pulmonary epithelial cells exposed to asbestos fibers.

Phosphorylation of p53 protein in A549 human pulmonary epithelial cells exposed to asbestos fibers.

Biological Effects of Asbestos Fibers on Human Cells In Vitro. Especially on Lymphocytes and Neutrophils.

Keynote lecture in the 13th Japanese Society of Immunotoxicology (JSIT 2006)

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