ArticleThe American journal of pathology2009
A protein kinase Cdelta-dependent protein kinase D pathway modulates ERK1/2 and JNK1/2 phosphorylation and Bim-associated apoptosis by asbestos.
Article in The American journal of pathology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
19 citing papers in PubMed, 31 citations in OpenAlex.
- Cycloastragenol in inflammation-related diseases: mechanisms, pharmacokinetics, and translational prospects.Frontiers in pharmacology · 2025Review
- Pathogenic Potential of Respirable Spodumene Cleavage Fragments following Application of Regulatory Counting Criteria for Asbestiform Fibres.International journal of environmental research and public health · 2022Article
- Mitochondria in Focus: From Function to Therapeutic Strategies in Chronic Lung Diseases.Frontiers in immunology · 2021Review
- The pathophysiological role of mitochondrial oxidative stress in lung diseases.Journal of translational medicine · 2017Review
- Asbestos-Induced Mesothelial to Fibroblastic Transition Is Modulated by the Inflammasome.The American journal of pathology · 2017Article
- The Role of Mitochondrial DNA in Mediating Alveolar Epithelial Cell Apoptosis and Pulmonary Fibrosis.International journal of molecular sciences · 2015Review
- The c-Jun N-terminal kinase signaling pathway mediates chrysotile asbestos-induced alveolar epithelial cell apoptosis.Molecular medicine reports · 2015Article
- Biliverdin reductase: a target for cancer therapy?Frontiers in pharmacology · 2015Review
- Oxidative stress and pulmonary fibrosis.Biochimica et biophysica acta · 2013Review
- Molecular basis of asbestos-induced lung disease.Annual review of pathology · 2013Review
- Biliverdin reductase: more than a namesake - the reductase, its Peptide fragments, and biliverdin regulate activity of the three classes of protein kinase C.Frontiers in pharmacology · 2012Article
- An extracellular signal-regulated kinase 2 survival pathway mediates resistance of human mesothelioma cells to asbestos-induced injury.American journal of respiratory cell and molecular biology · 2011Article
- ERK2 is essential for the growth of human epithelioid malignant mesotheliomas.International journal of cancer · 2011Article
- Role of mutagenicity in asbestos fiber-induced carcinogenicity and other diseases.Journal of toxicology and environmental health. Part B, Critical reviews · 2011Review
- Pulmonary endpoints (lung carcinomas and asbestosis) following inhalation exposure to asbestos.Journal of toxicology and environmental health. Part B, Critical reviews · 2011Review
- Protein kinase C and toll-like receptor signaling.Enzyme research · 2011Article
- Update in environmental and occupational medicine 2009.American journal of respiratory and critical care medicine · 2010Review
- Asbestos, lung cancers, and mesotheliomas: from molecular approaches to targeting tumor survival pathways.American journal of respiratory cell and molecular biology · 2010Review
- Utilization of gene profiling and proteomics to determine mineral pathogenicity in a human mesothelial cell line (LP9/TERT-1).Journal of toxicology and environmental health. Part A · 2010Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Inhalation of asbestos and oxidant-generating pollutants causes injury and compensatory proliferation of lung epithelium, but the signaling mechanisms that lead to these responses are unclear. We hypothesized that a protein kinase (PK)Cdelta-dependent PKD pathway was able to regulate downstream mitogen-activated protein kinases, affecting pro- and anti-apoptotic responses to asbestos. Elevated levels of phosphorylated PKD (p-PKD) were observed in distal bronchiolar epithelial cells of mice inhaling asbestos. In contrast, PKCdelta-/- mice showed significantly lower levels of p-PKD in lung homogenates and in situ after asbestos inhalation. In a murine lung epithelial cell line, asbestos caused significant increases in the phosphorylation of PKCdelta-dependent PKD, ERK1/2, and JNK1/2/c-Jun that occurred with decreases in the BH3-only pro-apoptotic protein, Bim. Silencing of PKCdelta, PKD, and use of small molecule inhibitors linked the ERK1/2 pathway to the prevention of Bim-associated apoptosis as well as the JNK1/2/c-Jun pathway to the induction of apoptosis. Our studies are the first to show that asbestos induces PKD phosphorylation in lung epithelial cells both in vivo and in vitro. PKCdelta-dependent PKD phosphorylation by asbestos is causally linked to a cellular pathway that involves the phosphorylation of both ERK1/2 and JNK1/2, which play opposing roles in the apoptotic response induced by asbestos.
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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.