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Molecular mechanisms of asbestos-induced lung epithelial cell apoptosis
Author(s):
Gang Liu
,
Rohinee Beri
,
Amanda Mueller
,
David W. Kamp
Publication date
Created:
November 2010
Publication date
(Print):
November 2010
Journal:
Chemico-Biological Interactions
Publisher:
Elsevier BV
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Abstract
Asbestos causes pulmonary fibrosis (asbestosis) and malignancies (bronchogenic lung cancer and mesothelioma) by mechanisms that are not fully elucidated. Accumulating evidence show that alveolar epithelial cell (AEC) apoptosis is a crucial initiating and perpetuating event in the development of pulmonary fibrosis following exposure to a wide variety of noxious stimuli, including asbestos. We review the important molecular mechanisms underlying asbestos-induced AEC apoptosis. Specifically, we focus on the role of asbestos in augmenting AEC apoptosis by the mitochondria- and p53-regulated death pathways that result from the production of iron-derived reactive oxygen species (ROS) and DNA damage. We summarize emerging evidence implicating the endoplasmic reticulum (ER) stress response in AEC apoptosis in patients with idiopathic pulmonary fibrosis (IPF), a disease with similarities to asbestosis. Finally, we discuss a recent finding that a mitochondrial oxidative DNA repair enzyme (8-oxoguanine DNA glycosylase; Ogg1) acts as a mitochondrial aconitase chaperone protein to prevent oxidant (asbestos and H(2)O(2))-induced AEC mitochondrial dysfunction and intrinsic apoptosis. The coupling of mitochondrial Ogg1 to mitochondrial aconitase is a novel mechanism linking metabolism to mitochondrial DNA that may be important in the pathophysiologic events resulting in oxidant-induced toxicity as seen in tumors, aging, and respiratory disorders (e.g. asbestosis, IPF). Collectively, these studies are illuminating the molecular basis of AEC apoptosis following asbestos exposure that may prove useful for developing novel therapeutic strategies. Importantly, the asbestos paradigm is elucidating pathophysiologic insights into other more common pulmonary diseases, such as IPF and lung cancer, for which better therapy is required. Copyright © 2010 Elsevier Ireland Ltd. All rights reserved.
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Inflamed lung in vitro co-culture models
Author and article information
Journal
Title:
Chemico-Biological Interactions
Abbreviated Title:
Chemico-Biological Interactions
Publisher:
Elsevier BV
ISSN (Print):
00092797
Publication date Created:
November 2010
Publication date (Print):
November 2010
Volume
: 188
Issue
: 2
Pages
: 309-318
Article
DOI:
10.1016/j.cbi.2010.03.047
PubMed ID:
20380827
SO-VID:
517f3c42-8c0d-42bd-80c0-b89d319b24a3
Copyright ©
© 2010
License:
https://www.elsevier.com/tdm/userlicense/1.0/
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