ArticleThe American journal of pathology2012
Targeted deletion of Jun/AP-1 in alveolar epithelial cells causes progressive emphysema and worsens cigarette smoke-induced lung inflammation.
Article in The American journal of pathology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 28 citations in OpenAlex.
- Article
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- Interaction of Biochemical Processes between Chronic Obstructive Pulmonary Disease (COPD), Pulmonary Arterial Hypertension (PAH), and Coronavirus Disease 2019 (COVID-19).Polish journal of microbiology · 2023Article
- A single-cell regulatory map of postnatal lung alveologenesis in humans and mice.Cell genomics · 2022Article
- Improving gene network inference with graph wavelets and making insights about ageing-associated regulatory changes in lungs.Briefings in bioinformatics · 2021Article
- Preconditioning the immature lung with enhanced Nrf2 activity protects against oxidant-induced hypoalveolarization in mice.Scientific reports · 2020Article
- Understanding the Early Biological Effects of Isoprene-Derived Particulate Matter Enhanced by Anthropogenic Pollutants.Research report (Health Effects Institute) · 2019Article
- Impaired calcium signaling in muscle fibers from intercostal and foot skeletal muscle in a cigarette smoke-induced mouse model of COPD.Muscle & nerve · 2017Article
- Gene Expression Profiling in Human Lung Cells Exposed to Isoprene-Derived Secondary Organic Aerosol.Environmental science & technology · 2017Article
- K-homology splicing regulatory protein (KSRP) promotes post-transcriptional destabilization of Spry4 transcripts in non-small cell lung cancer.The Journal of biological chemistry · 2017Article
- E3 ubiquitin ligase RFWD2 controls lung branching through protein-level regulation of ETV transcription factors.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Restoration of Corticosteroid Sensitivity in Chronic Obstructive Pulmonary Disease by Inhibition of Mammalian Target of Rapamycin.American journal of respiratory and critical care medicine · 2016Article
- Decreased Histone Deacetylase 2 (HDAC2) in Peripheral Blood Monocytes (PBMCs) of COPD Patients.PloS one · 2016Article
- Transcriptional profiling and targeted proteomics reveals common molecular changes associated with cigarette smoke-induced lung emphysema development in five susceptible mouse strains.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2015Article
- Myeloid-specific Fos-related antigen-1 regulates cigarette smoke-induced lung inflammation, not emphysema, in mice.American journal of respiratory cell and molecular biology · 2015Article
- Sirtuin 1 and aging theory for chronic obstructive pulmonary disease.Analytical cellular pathology (Amsterdam) · 2015Review
- Nuclear factor-kappa-B signaling in lung development and disease: one pathway, numerous functions.Birth defects research. Part A, Clinical and molecular teratology · 2014Review
- Neu-164 and Neu-107, two novel antioxidant and anti-myeloperoxidase compounds, inhibit acute cigarette smoke-induced lung inflammation.American journal of physiology. Lung cellular and molecular physiology · 2013Article
- Pathogenic mechanism of second hand smoke induced inflammation and COPD.Frontiers in physiology · 2012Article
Corrections and comments
- Erratum issuedCorrections.2017
Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Chronic obstructive pulmonary disease appears to occur slowly and progressively over many years, with both genetic factors and environmental modifiers contributing to its pathogenesis. Although the c-Jun/activator protein 1 transcriptional factor regulates cell proliferation, apoptosis, and inflammatory responses, its role in lung pathogenesis is largely unknown. In this study, we report decreased expression levels of c-Jun mRNA and protein in the lung tissues of patients with advanced chronic obstructive pulmonary disease, and the genetic deletion of c-Jun specifically in alveolar epithelial cells causes progressive emphysema with lung inflammation and alveolar air space enlargement, which are cardinal features of emphysema. Although mice lacking c-Jun specifically in lung alveolar epithelial cells appear normal at the age of 6 weeks, when exposed to long-term cigarette smoke, c-Jun-mutant mice display more lung inflammation with perivascular and peribronchiolar infiltrates compared with controls. These results demonstrate that the c-Jun/activator protein 1 pathway is critical for maintaining lung alveolar cell homeostasis and that loss of its expression can contribute to lung inflammation and progressive emphysema.
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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.