Asbestos-induced Disruption of Calcium Homeostasis Induces Endoplasmic Reticulum Stress in Macrophages
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Although the mechanisms for fibrosis development remain largely unknown, recent evidence indicates that endoplasmic reticulum (ER) stress and activation of the unfolded protein response (UPR) may act as an important fibrotic stimulus in diseased lungs. ER stress is observed in lungs of patients with idiopathic pulmonary fibrosis. In this study we evaluated if ER stress and the UPR was present in macrophages exposed to chrysotile asbestos and if ER stress in macrophages was associated with asbestos-induced pulmonary fibrosis. Macrophages exposed to chrysotile had elevated transcript levels of several ER stress genes. Macrophages loaded with the Ca(2+)-sensitive dye Fura2-AM showed that cytosolic Ca(2+) increased significantly within minutes after chrysotile exposure and remained elevated for a prolonged time. Chrysotile-induced increases in cytosolic Ca(2+) were partially inhibited by either anisomycin, an inhibitor of passive Ca(2+) leak from the ER, or 1,2-bis(2-aminophenoxyl)ethane-N,N,N',N'-tetraacetic acid (BAPTA-AM), an intracellular Ca(2+) chelator known to deplete ER Ca(2+) stores. Anisomycin inhibited X-box-binding protein 1 (XBP1) mRNA splicing and reduced immunoglobulin-binding protein (BiP) levels, whereas BAPTA-AM increased XBP1 splicing and BiP expression, suggesting that ER calcium depletion may be one factor contributing to ER stress in cells exposed to chrysotile. To evaluate ER stress in vivo, asbestos-exposed mice showed fibrosis development, and alveolar macrophages from fibrotic mice showed increased expression of BiP. Bronchoalveolar macrophages from asbestosis patients showed increased expression of several ER stress genes compared with normal subjects. These findings suggest that alveolar macrophages undergo ER stress, which is associated with fibrosis development.
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This latter pathway can account for the rapidity of changes in the metal concentration.
“This latter pathway can account for the rapidity of changes in the metal concentration [124].”
From Asbestos and Iron (2023) · cites this paper as [124]
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Munson, P. B. (2019) · ScholarWorks -A service of University of Vermont Libraries (University of Vermont) · Cited by 3 · see citing works
Morimoto, T., Izumi, H., Tomonaga, T., Nishida, C., Kawai, N., Higashi, Y., Wang, K., Ono, R., Sumiya, K., Sakurai, K., et al. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms25073573 · Cited by 3 · see citing works
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Chemical Modulation of AAV Trafficking
Berry, G. E. (2019) · Carolina Digital Repository (University of North Carolina at Chapel Hill) · doi:10.17615/dpe3-gy73
Richey, J. S., Shaw, J. R., Gupta, A. B., Fallacara, D. M., Sparrow, B., Wang, A., Elsass, K. E., Roberts, G., Yao, P., Stout, M. D., et al. (2025) · Journal of Occupational Medicine and Toxicology · doi:10.1186/s12995-025-00476-3
- Authors
- Ryan, A. J., Larson-Casey, J. L., He, C., Murthy, S., & Carter, A. B.
- Affiliations
- University of Iowa (US)
- Corresponding author
- Carter, A.Brent
- Venue
- Journal of Biological Chemistry
- Publisher
- Elsevier BV
- Published
- 2014-11
- Volume
- 289
- Issue
- 48
- Pages
- 33391-33403
- ISSN
- 0021-9258 (ISSN-L)
- PMC
- PMC4246095
- OpenAlex
- W2088671967
- Cited by
- 43
- References
- 53
- Citations by year
- 2025: 4 · 2024: 6 · 2023: 2 · 2021: 5 · 2020: 3 · 2019: 6 · 2018: 7 · 2017: 6 · 2016: 1 · 2015: 3
- FWCI
- 1.66
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Biological Chemistry (publishedVersion, cc-by)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (2 ROI ES 015981-08, P30 CA086862)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Endoplasmic Reticulum Stress and Disease
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Occupational and environmental lung diseases
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis
- Keywords
- asbestos, chrysotile, endoplasmic reticulum stress, unfolded protein response, pulmonary fibrosis, asbestosis, alveolar macrophages, calcium homeostasis, intracellular calcium, ER calcium depletion, XBP1 splicing, BiP, BAPTA-AM, anisomycin, idiopathic pulmonary fibrosis
- MeSH terms
- Regulatory Factor X Transcription Factors, X-Box Binding Protein 1, Adolescent, Adult, Animals, Asbestosis, Calcium, DNA-Binding Proteins, Female, Humans, Male, Pulmonary Fibrosis, RNA Splicing, Transcription Factors, Macrophages, Alveolar, Asbestos, Serpentine, Mice, Endoplasmic Reticulum Stress
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