ArticleEnvironmental health perspectives2009
Diesel exhaust particles activate the matrix-metalloproteinase-1 gene in human bronchial epithelia in a beta-arrestin-dependent manner via activation of RAS.
Article in Environmental health perspectives, 2009. 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 20 papers.
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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
20 citing papers in PubMed, 45 citations in OpenAlex.
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- Taurine ameliorates particulate matter-induced emphysema by switching on mitochondrial NADH dehydrogenase genes.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Transient Receptor Potential Vanilloid 4 Ion Channel Functions as a Pruriceptor in Epidermal Keratinocytes to Evoke Histaminergic Itch.The Journal of biological chemistry · 2016Article
- The impact of low-dose carcinogens and environmental disruptors on tissue invasion and metastasis.Carcinogenesis · 2015Review
- Keratinocyte growth regulation TRP-ed up over downregulated TRPV4?The Journal of investigative dermatology · 2014Article
- Emerging mechanistic targets in lung injury induced by combustion-generated particles.Toxicological sciences : an official journal of the Society of Toxicology · 2013Review
- Inflammation-related effects of diesel engine exhaust particles: studies on lung cells in vitro.BioMed research international · 2013Review
- β-Arrestin2 regulates lysophosphatidic acid-induced human breast tumor cell migration and invasion via Rap1 and IQGAP1.PloS one · 2013Article
- Multiple facets of cAMP signalling and physiological impact: cAMP compartmentalization in the lung.Pharmaceuticals (Basel, Switzerland) · 2012Article
- TRPV4 is a regulator of adipose oxidative metabolism, inflammation, and energy homeostasis.Cell · 2012Article
- Wider action plan and multidisciplinar approach could be a wining idea in creation of friendly environment.Journal of environmental and public health · 2012Article
- TRPV4-mediated calcium influx into human bronchial epithelia upon exposure to diesel exhaust particles.Environmental health perspectives · 2011Article
- β-arrestin deficiency protects against pulmonary fibrosis in mice and prevents fibroblast invasion of extracellular matrix.Science translational medicine · 2011Article
- Update in environmental and occupational medicine 2009.American journal of respiratory and critical care medicine · 2010Review
- Site controlled transgenic mice validating increased expression from human matrix metalloproteinase (MMP-1) promoter due to a naturally occurring SNP.Matrix biology : journal of the International Society for Matrix Biology · 2009Article
- Association ofIn vivo (Athens, Greece)Article
Corrections and comments
- Erratum issued
Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundDiesel exhaust particles (DEPs) are globally relevant air pollutants that exert a detrimental human health impact. However, mechanisms of damage by DEP exposure to human respiratory health and human susceptibility factors are only partially known. Matrix metalloproteinase-1 (MMP-1) has been implied as an (etio)pathogenic factor in human lung and airway diseases such as emphysema, chronic obstructive pulmonary disease, chronic asthma, tuberculosis, and bronchial carcinoma and has been reported to be regulated by DEPs.
objectiveWe elucidated the molecular mechanisms of DEPs' up-regulation of MMP-1. METHODS/
resultsUsing permanent and primary human bronchial epithelial (HBE) cells at air-liquid interface, we show that DEPs activate the human MMP-1 gene via RAS and subsequent activation of RAF-MEK-ERK1/2 mitogen-activated protein kinase signaling, which can be scaffolded by beta-arrestins. Short interfering RNA mediated beta-arrestin1/2 knockout eliminated formation, subsequent nuclear trafficking of phosphorylated ERK1/2, and resulting MMP-1 transcriptional activation. Transcriptional regulation of the human MMP-1 promoter was strongly influenced by the presence of the -1607GG polymorphism, present in 60-80% of humans, which led to striking up-regulation of MMP-1 transcriptional activation.
conclusionOur results confirm up-regulation of MMP-1 in response to DEPs in HBE and provide new mechanistic insight into how these epithelia, the first line of protection against environmental insults, up-regulate MMP-1 in response to DEP inhalation. These mechanisms include a role for the human -1607GG polymorphism as a susceptibility factor for an accentuated response, which critically depends on the ability of beta-arrestin1/2 to generate scaffolding and nuclear trafficking of phosphorylated ERK1/2.
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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.