Gene Expression Profiles Reveal Increased mClca3 (Gob5) Expression and Mucin Production in a Murine Model of Asbestos-Induced Fibrogenesis
Open accessAbstract
To elucidate genes important in development or repair of asbestos-induced lung diseases, gene expression was examined in mice after inhalation of chrysotile asbestos for 3, 9, and 40 days. We identified changes in the expression of genes linked to proliferation (cyclin B2, CDC20, and CDC28 protein kinase regulatory subunit 2), inflammation (CCL9, CCL6, complement component 1, chitinase3-like 3, TNF superfamily member 10, and IL-1B), and matrix remodeling (MMP12, MMP3, integrin alphaX, and cathepsins K, Z, B, and S). The most highly induced gene at all time points was mclca3 (gob5), a putative calcium-activated chloride channel involved in the regulation of mucus production and/or secretion. Using histochemistry, we demonstrated accumulation of mucus and increased mClca3 protein in the bronchiolar epithelium of asbestos-exposed mice at all time points but peaking at 9 days. Cytokine levels (interleukin-1beta, interleukin-4, interleukin-6) in bronchoalveolar lavage fluid also increased at 9 days, suggesting Th2-mediated immunity may play a role in asbestos-induced mucus production. In contrast, levels of cathepsin K, a potent elastase, increased between 3 and 40 days at both the mRNA and protein levels, localizing primarily in CD45-positive leukocytes and interstitial cells. Identification of genes involved in lung injury and remodeling after asbestos exposure could aid in defining mechanisms of airborne particulate-induced disease and in developing therapeutic strategies.
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Asbestos increased mucin production to a similar extent in lungs of both Nalp3-/- and Nalp3+/+ mice.
“Although mucin production, which parallels inflammatory changes in lungs and may occur to facilitate clearance of asbestos fibers (21), was similarly increased by asbestos in Nalp3 -/-and Nalp3 +/+ lungs, significant increases in the number of mucinproducing distal bronchioles, sites of impact of chrysotile asbestos fibers after inhalation, occurred in Nalp3 -/-mice (table S1).”
From Innate Immune Activation Through Nalp3 Inflammasome Sensing of Asbestos and Silica (2008) · cites this paper as [21]
Nalp3-/- mice showed a significant rise in the count of mucin-producing distal bronchioles.
“Although mucin production, which parallels inflammatory changes in lungs and may occur to facilitate clearance of asbestos fibers (21), was similarly increased by asbestos in Nalp3 -/-and Nalp3 +/+ lungs, significant increases in the number of mucinproducing distal bronchioles, sites of impact of chrysotile asbestos fibers after inhalation, occurred in Nalp3 -/-mice (table S1).”
From Innate Immune Activation Through Nalp3 Inflammasome Sensing of Asbestos and Silica (2008) · cites this paper as [21]
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Innate Immune Activation Through Nalp3 Inflammasome Sensing of Asbestos and Silica
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- Authors
- Sabo-Attwood, T., Ramos-Nino, M., Bond, J., Butnor, K. J., Heintz, N., Gruber, A. D., Steele, C., Taatjes, D. J., Vacek, P., & Mossman, B. T.
- Affiliations
- University of Vermont (US)
- Freie Universität Berlin (DE)
- Children's Hospital of Pittsburgh (US)
- Corresponding author
- Mossman, Brooke T.
- Venue
- The American Journal of Pathology
- Publisher
- Elsevier BV
- Published
- 2005-11
- Volume
- 167
- Issue
- 5
- Pages
- 1243-1256
- ISSN
- 0002-9440 (ISSN-L)
- PMC
- PMC1603789
- OpenAlex
- W2019843033
- Cited by
- 72
- References
- 67
- Citations by year
- 2026: 2 · 2024: 1 · 2023: 4 · 2022: 2 · 2020: 3 · 2019: 4 · 2017: 6 · 2016: 3 · 2015: 4 · 2014: 6 · 2013: 3 · 2012: 5
- FWCI
- 5.33
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- American Journal Of Pathology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- University of Pittsburgh
- University of Vermont
- National Heart, Lung, and Blood Institute (P01HL067004, HL67004)
- National Institute of Environmental Health Sciences (T32 ES07122, T32ES007122)
- Topics
- 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
- Social Sciences › Health › Occupational Health and Global Justice
- Keywords
- chrysotile, calcium-activated chloride channels, mucus production, mucin, bronchiolar epithelium, Th2 immune response, cathepsin K, elastase, matrix remodeling, inflammation, gene expression profiling, lung injury, mouse model
- MeSH terms
- Animals, Asbestos, Asbestosis, Bronchoalveolar Lavage Fluid, Disease Models, Animal, Immunohistochemistry, Male, Mice, Inbred C57BL, Mucins, Mucoproteins, Pancreatic Elastase, Pulmonary Fibrosis, RNA, Messenger, Gene Expression, Cytokines, Chloride Channels, Oligonucleotide Array Sequence Analysis, Respiratory Mucosa, Gene Expression Profiling, Mice
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