ArticleJournal of thoracic disease2016
Proteomic profiling change during the early development of silicosis disease.
Article in Journal of thoracic disease, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 19 citations in OpenAlex.
- A Multi-omics Framework Combining Genomics and Proteomics for Silicosis Prediction in Chinese Workers - Jiangsu Province, China, 2023-2024.China CDC weekly · 2025Article
- Metabolomics and proteomics in occupational medicine: a comprehensive systematic review.Journal of occupational medicine and toxicology (London, England) · 2024Review
- Article
- Prolonged Inhalation Exposure to Coal Dust on Irradiated Rats and Consequences.TheScientificWorldJournal · 2022Article
- Early Detection Methods for Silicosis in Australia and Internationally: A Review of the Literature.International journal of environmental research and public health · 2021Review
- Dynamic assessing silica particle-induced pulmonary fibrosis and associated regulation of long non-coding RNA expression in Wistar rats.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 2021Article
- CircHECTD1 mediates pulmonary fibroblast activationTherapeutic advances in chronic disease · 2019Article
- Emerging Role of Immunosuppression in Diseases Induced by Micro- and Nano-Particles: Time to Revisit the Exclusive Inflammatory Scenario.Frontiers in immunology · 2018Review
- Serum concentrations of Krebs von den Lungen-6, surfactant protein D, and matrix metalloproteinase-2 as diagnostic biomarkers in patients with asbestosis and silicosis: a case-control study.BMC pulmonary medicine · 2017Article
- Inflammatory biomarkers in workers exposed to silica dust: integrative review.Revista brasileira de medicina do trabalho : publicacao oficial da Associacao Nacional de Medicina do Trabalho-ANAMTReview
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundSilicosis is one of several severe occupational diseases for which effective diagnostic tools during early development are currently unavailable. In this study we focused on proteomic profiling during the early stages of silicosis to investigate the pathophysiology and identify the proteins involved.
methodsTwo-dimensional (2D) gel electrophoresis and MALDI-TOF-MS were used to assess the proteomic differences between healthy individuals (HI), dust-exposed workers without silicosis (DEW) and silicosis patients (SP). Proteins abundances that differed by a factor of two-fold or greater were subjected to more detailed analysis, and enzyme linked to immunosorbent assay (ELISA) was employed to correlate with protein expression data.
resultsCompared with HI, 42 proteins were more abundant and 8 were less abundant in DEW, and these were also differentially accumulated in SP. Closer inspection revealed that serine protease granzyme A, alpha-1-B-glycoprotein (A1BG) and the T4 surface glycoprotein precursor (TSGP) were among the up-regulated proteins in DEW and SP. Significant changes in serine proteases, glycoproteins and proto-oncogenes may be associated with the response to cytotoxicity and infectious pathogens by activation of T cells, positive regulation of extracellular matrix structural constituents and immune response, and fibroblast proliferation. Up-regulation of cytokines included TNFs, interferon beta precursor, interleukin 6, atypical chemokine receptor 2, TNFR13BV, and mutant IL-17F may be involved in the increased and persistent immune response and fibrosis that occurred during silicosis development.
conclusionsGranzymes, glycoproteins, cytokines and immune factors were dramatically involved in the immune response, metabolism, signal regulation and fibrosis during the early development of silicosis. Proteomic profiling has expanded our understanding of the pathogenesis of silicosis, and identified a number of targets that may be potential biomarkers for early diagnosis of this debilitating disease.
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