ArticleThe American journal of pathology2000
Increased phosphorylated extracellular signal-regulated kinase immunoreactivity associated with proliferative and morphologic lung alterations after chrysotile asbestos inhalation in mice.
Article in The American journal of pathology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
21 citing papers in PubMed, 77 citations in OpenAlex.
- Cellular defense mechanisms against asbestos fibers.Frontiers in public health · 2025Review
- Regulatory role of heme oxygenase-1 in silica-induced lung injury.Respiratory research · 2018Article
- Subchronic pulmonary pathology, iron overload, and transcriptional activity after Libby amphibole exposure in rat models of cardiovascular disease.Environmental health perspectives · 2012Article
- Osteopontin modulates inflammation, mucin production, and gene expression signatures after inhalation of asbestos in a murine model of fibrosis.The American journal of pathology · 2011Article
- Pulmonary endpoints (lung carcinomas and asbestosis) following inhalation exposure to asbestos.Journal of toxicology and environmental health. Part B, Critical reviews · 2011Review
- Asbestos, lung cancers, and mesotheliomas: from molecular approaches to targeting tumor survival pathways.American journal of respiratory cell and molecular biology · 2010Review
- A protein kinase Cdelta-dependent protein kinase D pathway modulates ERK1/2 and JNK1/2 phosphorylation and Bim-associated apoptosis by asbestos.The American journal of pathology · 2009Article
- Innate immune activation through Nalp3 inflammasome sensing of asbestos and silica.Science (New York, N.Y.) · 2008Article
- Targeting the MEK1 cascade in lung epithelium inhibits proliferation and fibrogenesis by asbestos.American journal of respiratory cell and molecular biology · 2008Article
- The role of inflammation in the pathogenesis of idiopathic pulmonary fibrosis.Antioxidants & redox signaling · 2008Review
- Decreased asbestos-induced lung inflammation and fibrosis after radiation and bone marrow transplant.American journal of respiratory cell and molecular biology · 2008Article
- Laser capture microdissection reveals dose-response of gene expression in situ consequent to asbestos exposure.International journal of experimental pathology · 2007Article
- Asbestos-induced peribronchiolar cell proliferation and cytokine production are attenuated in lungs of protein kinase C-delta knockout mice.The American journal of pathology · 2007Article
- Gene expression profiles reveal increased mClca3 (Gob5) expression and mucin production in a murine model of asbestos-induced fibrogenesis.The American journal of pathology · 2005Article
- Src-dependent ERK5 and Src/EGFR-dependent ERK1/2 activation is required for cell proliferation by asbestos.Oncogene · 2004Article
- Phosphorylation state-specific antibodies: applications in investigative and diagnostic pathology.The American journal of pathology · 2003Review
- Phosphorylation of p53 protein in A549 human pulmonary epithelial cells exposed to asbestos fibers.Environmental health perspectives · 2003Article
- Persistent localization of activated extracellular signal-regulated kinases (ERK1/2) is epithelial cell-specific in an inhalation model of asbestosis.The American journal of pathology · 2003Article
- Increased localization and substrate activation of protein kinase C delta in lung epithelial cells following exposure to asbestos.The American journal of pathology · 2002Article
- Assessing nanotoxicity in cells in vitro.Wiley interdisciplinary reviews. Nanomedicine and nanobiotechnologyReview
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Activation of extracellular signal-regulated kinases (ERK) has been associated with the advent of asbestos-associated apoptosis and proliferation in mesothelial and alveolar epithelial cells and may be linked to the development of pulmonary fibrosis. The objective of studies here was to characterize the development of inflammation, cellular proliferation, and fibrosis in asbestos-exposed C57Bl/6 mice in relationship to patterns of ERK phosphorylation. Inflammation occurred after 10 and 20 days of asbestos exposure as evidenced by increases in total protein and neutrophils in bronchoalveolar lavage fluid. Increases in cell proliferation were observed at 30 days in bronchiolar epithelia and at 4, 14, and 30 days in the alveolar compartment of the lung. Trichrome-positive focal lesions of pulmonary fibrosis developed at 30 days in the absence of elevations in lung hydroxyproline or procollagen mRNA levels. Striking increases in ERK phosphorylation were observed within pulmonary epithelial cells at sites of developing fibrotic lesions after 14 and 30 days of inhalation. In addition to characterizing a murine inhalation model of asbestosis, we provide the first evidence showing activation of ERK signaling within lung epithelium in vivo, following inhalation of asbestos fibers.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.