ArticleParticle and fibre toxicology2014
Asbestos modulates thioredoxin-thioredoxin interacting protein interaction to regulate inflammasome activation.
Article in Particle and fibre toxicology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 42 citations in OpenAlex.
- NLRP3 inflammasome activation by particles and fibers: implications for human hazard assessment.Archives of toxicology · 2026Review
- Cellular defense mechanisms against asbestos fibers.Frontiers in public health · 2025Review
- TXNIP regulates pulmonary inflammation induced by Asian sand dust.Redox biology · 2024Article
- Asbestos-induced chronic inflammation in malignant pleural mesothelioma and related therapeutic approaches-a narrative review.Precision cancer medicine · 2021Article
- CRP-Induced NLRP3 Inflammasome Activation Increases LDL Transcytosis Across Endothelial Cells.Frontiers in pharmacology · 2019Article
- Exosomes from asbestos-exposed cells modulate gene expression in mesothelial cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018Article
- Analysis of autoantibody profiles in two asbestiform fiber exposure cohorts.Journal of toxicology and environmental health. Part A · 2018Article
- Actin polymerization plays a significant role in asbestos-induced inflammasome activation in mesothelial cells in vitro.Histochemistry and cell biology · 2017Article
- Asbestos-Induced Mesothelial to Fibroblastic Transition Is Modulated by the Inflammasome.The American journal of pathology · 2017Article
- Mitochondrial catalase overexpressed transgenic mice are protected against lung fibrosis in part via preventing alveolar epithelial cell mitochondrial DNA damage.Free radical biology & medicine · 2016Article
- The NLRP3 inflammasome in pathogenic particle and fibre-associated lung inflammation and diseases.Particle and fibre toxicology · 2016Review
- The complex cascade of cellular events governing inflammasome activation and IL-1β processing in response to inhaled particles.Particle and fibre toxicology · 2016Review
- Diverse properties of the mesothelial cells in health and disease.Pleura and peritoneum · 2016Review
- Article
- Asbestos Induces Oxidative Stress and Activation of Nrf2 Signaling in Murine Macrophages: Chemopreventive Role of the Synthetic Lignan Secoisolariciresinol Diglucoside (LGM2605).International journal of molecular sciences · 2016Article
- Cigarette smoke represses the innate immune response to asbestos.Physiological reports · 2015Article
- Current Research and Opportunities to Address Environmental Asbestos Exposures.Environmental health perspectives · 2015Article
- The cysteine proteome.Free radical biology & medicine · 2015Review
- Systemic autoimmune disease in asbestosis rapidly responding to anti-interleukin-1beta antibody canakinumab: a case report.BMC musculoskeletal disorders · 2015Article
- Indications for distinct pathogenic mechanisms of asbestos and silica through gene expression profiling of the response of lung epithelial cells.Human molecular genetics · 2015Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
backgroundAsbestos exposure is related to various diseases including asbestosis and malignant mesothelioma (MM). Among the pathogenic mechanisms proposed by which asbestos can cause diseases involving epithelial and mesothelial cells, the most widely accepted one is the generation of reactive oxygen species and/or depletion of antioxidants like glutathione. It has also been demonstrated that asbestos can induce inflammation, perhaps due to activation of inflammasomes.
methodsThe oxidation state of thioredoxin was analyzed by redox Western blot analysis and ROS generation was assessed spectrophotometrically as a read-out of solubilized formazan produced by the reduction of nitrotetrazolium blue (NTB) by superoxide. Quantitative real time PCR was used to assess changes in gene transcription.
resultsHere we demonstrate that crocidolite asbestos fibers oxidize the pool of the antioxidant, Thioredoxin-1 (Trx1), which results in release of Thioredoxin Interacting Protein (TXNIP) and subsequent activation of inflammasomes in human mesothelial cells. Exposure to crocidolite asbestos resulted in the depletion of reduced Trx1 in human peritoneal mesothelial (LP9/hTERT) cells. Pretreatment with the antioxidant dehydroascorbic acid (a reactive oxygen species (ROS) scavenger) reduced the level of crocidolite asbestos-induced Trx1 oxidation as well as the depletion of reduced Trx1. Increasing Trx1 expression levels using a Trx1 over-expression vector, reduced the extent of Trx1 oxidation and generation of ROS by crocidolite asbestos, and increased cell survival. In addition, knockdown of TXNIP expression by siRNA attenuated crocidolite asbestos-induced activation of the inflammasome.
conclusionOur novel findings suggest that extensive Trx1 oxidation and TXNIP dissociation may be one of the mechanisms by which crocidolite asbestos activates the inflammasome and helps in development of MM.
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