Subchronic inhalation of coal dust particulate matter 10 induces bronchoalveolar hyperplasia and decreases MUC5AC expression in male Wistar rats

Kania, Nia; Setiawan, Bambang; Widjadjanto, Edi; Nurdiana, Nurdiana; Widodo, M. Aris; Kusuma, H.M.S. Chandra

doi:10.1016/j.etp.2014.06.001

Cited by 9 publications

(8 citation statements)

References 15 publications

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“…Labelling immunofluorescence was carried out according to the protocol in the previous study [ 22 ]. Antibodies used include anti-Caspase-3 mouse monoclonal antibody (Santa Cruz Biotechnology, Dallas, Texas, US), anti Ki67 rabbit polyclonal antibody (Santa Cruz Biotechnology, Dallas, Texas, US), anti-Mucin 2 rabbit polyclonal antibody (Santa Cruz Biotechnology, Dallas, Texas, US), anti-NFkB mouse monoclonal antibody (Santa Cruz Biotechnology, Dallas, Texas, US).…”

Section: Methodsmentioning

confidence: 99%

Decreased expression of MUC2 due to a decrease in the expression of lectins and apoptotic defects in colitis patients

Wibowo

Pardjianto

Sumitro

et al. 2019

Biochemistry and Biophysics Reports

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Introduction The involvement of mucin, lectin, and apoptosis in colitis is still unclear. This study aimed to investigate changes in MUC2 expression, inflammation, and changes in lectin expression in colitis patients. Methods A total of 17 patients were divided into two groups including 11 hemorrhoid patients as a control group and 6 colitis patients. MUC2 mutation analysis was carried out using immunofluorescent and FISH techniques. Assessment of caspase-3, Ki-67, NF-kB, and lectin expressions was also carried out by immunofluorescent technique then analyzed by confocal laser scanning microscope. Results The MUC2, caspase-3, and lectin expressions were significantly lower in the colitis group than in the control group (p < 0.05). Conclusions It was concluded that in colitis there was a change in MUC2 expression due to changes in lectins accompanied by apoptotic defects.conclusion

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Section: Methodsmentioning

confidence: 99%

Decreased expression of MUC2 due to a decrease in the expression of lectins and apoptotic defects in colitis patients

Wibowo

Pardjianto

Sumitro

et al. 2019

Biochemistry and Biophysics Reports

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Section: Introductionmentioning

confidence: 99%

“…Continued exposure to high concentrations of coal dust may lead to an inability to remove accumulated dust particles, resulting in structural damage to the alveoli [ 11 ]. Alveolar epithelial cells are the primary functional unit for O 2 exchange and the first point of contact for inhaled particles [ 11 ]. Successful alveolar epithelial repair and functional recovery require the proliferation and differentiation of alveolar type 2 stem/progenitor cells (AT2).…”

Section: Introductionmentioning

confidence: 99%

Coal dust exposure triggers heterogeneity of transcriptional profiles in mouse pneumoconiosis and Vitamin D remedies

Zou

et al. 2022

Part Fibre Toxicol

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Background Coal dust particles (CDP), an inevitable by-product of coal mining for the environment, mainly causes coal workers’ pneumoconiosis (CWP). Long-term exposure to coal dust leads to a complex alternation of biological processes during regeneration and repair in the healing lung. However, the cellular and complete molecular changes associated with pulmonary homeostasis caused by respiratory coal dust particles remain unclear. Methods This study mainly investigated the pulmonary toxicity of respirable-sized CDP in mice using unbiased single-cell RNA sequencing. CDP (< 5 μm) collected from the coal mine was analyzed by Scanning Electron Microscope (SEM) and Mass Spectrometer. In addition, western blotting, Elisa, QPCR was used to detect gene expression at mRNA or protein levels. Pathological analysis including HE staining, Masson staining, immunohistochemistry, and immunofluorescence staining were performed to characterize the structure and functional alternation in the pneumoconiosis mouse and verify the reliability of single-cell sequencing results. Results SEM image and Mass Spectrometer analysis showed that coal dust particles generated during coal mine production have been crushed and screened with a diameter of less than 5 µm and contained less than 10% silica. Alveolar structure and pulmonary microenvironment were destroyed, inflammatory and death (apoptosis, autophagy, and necrosis) pathways were activated, leading to pneumoconiosis in post 9 months coal dust stimulation. A distinct abnormally increased alveolar type 2 epithelial cell (AT2) were classified with a highly active state but reduced the antimicrobial-related protein expression of LYZ and Chia1 after CDP exposure. Beclin1, LC3B, LAMP2, TGF-ß, and MLPH were up-regulated induced by CDP, promoting autophagy and pulmonary fibrosis. A new subset of macrophages with M2-type polarization double expressed MLPH + /CD206 + was found in mice having pneumoconiosis but markedly decreased after the Vitamin D treatment. Activated MLPH + /CD206 + M2 macrophages secreted TGF-β1 and are sensitive to Vitamin D treatment. Conclusions This is the first study to reconstruct the pathologic progression and transcriptome pattern of coal pneumoconiosis in mice. Coal dust had obvious toxic effects on lung epithelial cells and macrophages and eventually induced pulmonary fibrosis. CDP-induced M2-type macrophages could be inhibited by VD, which may be related to the alleviation of the pulmonary fibrosis process.

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“…The diversity of macrophages differentiates in coal pneumoconiosis, and the long-term coal dust-induced alveolar in ammatory mechanism remains unclear. Respiratory dysfunction and continued exposure to high concentrations of coal dust may lead to an inability to remove accumulated coal dust particles, resulting in structural damage to the alveoli [12], a signi cant challenge for alveolar epithelial repair and functional recovery. Alveolar epithelial cells are the primary functional unit for O 2 exchange and the rst point of contact for inhaled particles [12].…”

mentioning

confidence: 99%

“…Respiratory dysfunction and continued exposure to high concentrations of coal dust may lead to an inability to remove accumulated coal dust particles, resulting in structural damage to the alveoli [12], a signi cant challenge for alveolar epithelial repair and functional recovery. Alveolar epithelial cells are the primary functional unit for O 2 exchange and the rst point of contact for inhaled particles [12]. Although signi cant regeneration of alveolar epithelial cells has been reported, and this regeneration process leads to dysplasia or developmental delays in repair [13].…”

mentioning

confidence: 99%

Coal Dust Exposure Triggers Heterogeneity of Transcriptional Profiles in Mouse Pneumoconiosis and Vitamin D Remedies

Zou

et al. 2021

Preprint

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Background: Coal dust particles (CDP), an inevitable by-product of coal mining for the environment, mainly causes coal workers’ pneumoconiosis (CWP). Long-term exposure to coal dust leads to a complex alternation of biological processes during regeneration and repair in the healing lung. However, the cellular and molecular mechanism of abnormal homeostasis in lung tissue are not explicit. Methods: This study mainly investigated the pulmonary toxicity of respirable-sized CDP in mice using unbiased single-cell RNA sequencing. CDP (less than 5μm) collected from the coal mine was analyzed by Scanning Electron Microscope (SEM) and Mass Spectrometer. In addition, western blotting, Elisa, QPCR was used to detect gene expression at mRNA or protein levels. Pathological analysis including HE staining, Masson staining, immunohistochemistry, and immunofluorescence staining were performed to characterize the structure and functional alternation in the pneumoconiosis mouse and verify the reliability of single-cell sequencing results.Results: SEM image and Mass Spectrometer analysis showed that coal dust particles generated during coal mine production have been crushed and screened with a diameter of less than 5 µm and contained less than 10% silica. Dust can intranasally enter the alveoli in mice. Compared with the control group, alveolar epithelial cells and macrophages showed apparent heterogeneity after long-term exposure to CDP. Alveolar structure and pulmonary microenvironment were destroyed, leading to pneumoconiosis after coal dust stimulation. A distinct abnormally increased 39 population of alveolar type 2 epithelial cells (AT2) was classified with a highly active state but reducing the antimicrobial-related protein expression of LYZ and Chia1 after CDP exposure. Unique 40 inflammatory factors and signaling pathways further characterized critical signal exchanges between epithelial cells and macrophages. Apoptosis, autophagy and necrosis pathways were activated. A new subset of macrophages with M2-type polarization double expressed MLPH+/CD206+ was found in mice having pneumoconiosis but markedly decreased after the vitamin D treatment. Activated MLPH+/CD206+ M2 macrophages secreted TGF-β1 and are sensitive to vitamin D treatment. Beclin1, LC3B, LAMP2, TGF-ß, and MLPH were up-regulated, promoting autophagy and pulmonary fibrosis. Vitamin D supplements can reduce the cytotoxicity induced by CDP. This study first reconstructed the pathologic progression and transcriptome landscape of coal-pneumoconiosis and the therapeutic opportunity of vitamin D in mice.

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Subchronic inhalation of coal dust particulate matter 10 induces bronchoalveolar hyperplasia and decreases MUC5AC expression in male Wistar rats

Cited by 9 publications

References 15 publications

Decreased expression of MUC2 due to a decrease in the expression of lectins and apoptotic defects in colitis patients

Decreased expression of MUC2 due to a decrease in the expression of lectins and apoptotic defects in colitis patients

Coal dust exposure triggers heterogeneity of transcriptional profiles in mouse pneumoconiosis and Vitamin D remedies

Coal Dust Exposure Triggers Heterogeneity of Transcriptional Profiles in Mouse Pneumoconiosis and Vitamin D Remedies

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