Background: Silicosis is a severe occupational disease characterized by pulmonary fibrosis, whereas chronic bronchitis (CB) is an acute inflammation of the airways. Differences in the mechanisms of pathogenesis of these diseases are not well understood, therefore we performed proteomic profiling of silicosis and CB patients and, compared the results.
Methods: Two-dimensional gel electrophoresis and MALDI-TOF-MS (matrix assisted laser desorption ionization time of flight mass spectrometry) were used to identify differentially accumulated proteins in stage I of silicosis (SI), stage II of silicosis (SII) and CB. Enzyme linked immunosorbent assay (ELISA) was employed to validate protein expression data.
Results: A total of 28 and 10 proteins were up- and down-regulated in SI, and 21 and 9 proteins were up- and down-regulated SII, compared with CB. Transforming growth factor beta-1 precursor and interferon beta precursor were up-regulated in CB, while interleukin 6, tumor necrosis factor (TNF) and a variant TNF receptor 13B were down-regulated in CB. Additionally, glycoprotein- and apolipoprotein-associated proteins including apolipoprotein A-IV and α-1-B-glycoprotein were up-regulated in CB, indicating an involvement in the pathogenesis of CB but not silicosis. By contrast, HLA-DRB1, medullasin and the proto-oncogene c-Fos were up-regulated in CB.
Conclusions: The immune, metabolism and apolipoprotein-related proteins were identified as playing specific and different roles in silicosis and CB. These proteomic profiling differences would facilitate further studies on the mechanisms underlying silicosis and CB, and may also prove useful to disease diagnosis and treatments.
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http://dx.doi.org/10.21037/jtd.2016.02.68 | DOI Listing |
Cytotechnology
April 2025
University Centre for Research and Development, University Institute of Pharmaceutical Sciences, Chandigarh University, Gharuan, Mohali, 140413 India.
When juxtaposed with 2D cell culture models, multicellular tumor spheroids demonstrate a capacity to faithfully replicate certain features inherent to solid tumors. These include spatial architecture, physiological responses, the release of soluble mediators, patterns of gene expression, and mechanisms of drug resistance. The morphological and behavioural similarities between 3D-cultured cells and cells within tumor masses highlight the potential of these models in studying cancer biology and drug responses.
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January 2025
Department of Chemistry, Pohang University of Science and Technology (POSTECH), Pohang 37673, Republic of Korea.
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Department of Oncology, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan Province, China.
Epithelial ovarian cancer (EOC) is the most lethal gynecologic malignancy which mainly consists of serous, mucinous, clear cell, and endometrioid subtypes. Due to the lack of classic symptoms at an early stage, EOC usually presented as advanced tumors with local and/or distant metastasis. Although a large portion of EOC was initially platinum-sensitive, most patients would acquire resistance to common chemotherapeutic agents.
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January 2025
Department of Oral and Maxillofacial Pathology and Microbiology, Manipal College of Dental Sciences, Manipal Academy of Higher Education, Manipal, 576104, India.
Oral submucous fibrosis (OSF) is a chronic, progressive, and fibrotic condition of the oral mucosa that carries an elevated risk of malignant transformation. We aimed to identify and validate novel genes associated with the regulation of epithelial-to-mesenchymal transition (EMT) in OSF. Genes regulating EMT were identified through differential gene expression analysis, using a LogFC threshold of -1 and + 1 and a padj value < 0.
View Article and Find Full Text PDFSci Rep
January 2025
Graduate Course in Medicine (Pathological Anatomy), Federal University of Rio de Janeiro, Rio de Janeiro, Brazil.
Muscular dystrophies (MD) are a group of hereditary diseases marked by progressive muscle loss, leading to weakness and degeneration of skeletal muscles. These conditions often result from structural defects in the Dystrophin-Glycoprotein Complex (DGC), as seen in Duchenne Muscular Dystrophy (DMD) and Becker Muscular Dystrophy (BMD). Since MDs currently have no cure, research has focused on identifying potential therapeutic targets to improve patients' quality of life.
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