ArticleThe American journal of pathology2002
Increased localization and substrate activation of protein kinase C delta in lung epithelial cells following exposure to asbestos.
Article in The American journal of pathology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 33 citations in OpenAlex.
- The Role of Mitochondrial DNA in Mediating Alveolar Epithelial Cell Apoptosis and Pulmonary Fibrosis.International journal of molecular sciences · 2015Review
- PKCδ/midkine pathway drives hypoxia-induced proliferation and differentiation of human lung epithelial cells.American journal of physiology. Cell physiology · 2014Article
- Oxidative stress and pulmonary fibrosis.Biochimica et biophysica acta · 2013Review
- Molecular basis of asbestos-induced lung disease.Annual review of pathology · 2013Review
- PKC activation induces inflammatory response and cell death in human bronchial epithelial cells.PloS one · 2013Article
- Ectopic ERK expression induces phenotypic conversion of C10 cells and alters DNA methyltransferase expression.BMC research notes · 2012Article
- Activated cAMP response element binding protein is overexpressed in human mesotheliomas and inhibits apoptosis.The American journal of pathology · 2009Article
- Protein kinase C delta regulates airway mucin secretion via phosphorylation of MARCKS protein.The American journal of pathology · 2007Article
- Gene expression profiles in asbestos-exposed epithelial and mesothelial lung cell lines.BMC genomics · 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
- Organ distribution of severe acute respiratory syndrome (SARS) associated coronavirus (SARS-CoV) in SARS patients: implications for pathogenesis and virus transmission pathways.The Journal of pathology · 2004Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The protein kinase C (PKC) family consists of several isozymes whose substrates may be necessary for the regulation of key cellular events important in the pathogenesis of proliferative diseases. Asbestos is a carcinogen and fibroproliferative agent in lung that may cause cell signaling events through activation of PKC. Here we used a murine inhalation model of asbestos-induced inflammation and fibrosis to examine immunoreactivity of PKC delta and its substrate, phosphorylated-adducin (p-adducin), in cells of the lung. Moreover, we characterized PKC delta and p-adducin expression in a pulmonary epithelial cell line (C10) in both log versus confluent cells and in cells after mechanical wounding or crocidolite asbestos exposure. Both PKC delta and p-adducin were almost exclusively expressed in bronchiolar and alveolar type II (ATII) epithelial cells in lung sections and increased in these cell types after inhalation of asbestos by mice. Increases in membrane and nuclear localization of PKC delta were seen in log phase as compared to confluent C10 cells. Moreover, enhanced immunoreactivity of PKC delta was observed in epithelial cells expressing proliferating cell nuclear antigen (PCNA) after mechanical wounding or exposure to asbestos fibers. These studies show that activated PKC delta in pulmonary epithelial cells is a consequence of inhalation of asbestos and may be linked to the activation of cell proliferation.
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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.