ArticleAmerican journal of respiratory cell and molecular biology2012
Nickel nanoparticles enhance platelet-derived growth factor-induced chemokine expression by mesothelial cells via prolonged mitogen-activated protein kinase activation.
Article in American journal of respiratory cell and molecular biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 32 citations in OpenAlex.
- The pulmonary effects of nickel-containing nanoparticles: Cytotoxicity, genotoxicity, carcinogenicity, and their underlying mechanisms.Environmental science. Nano · 2024Article
- Nickel Nanoparticles Induced Hepatotoxicity in Mice via Lipid-Metabolism-Dysfunction-Regulated Inflammatory Injury.Molecules (Basel, Switzerland) · 2023Article
- Nickel nanoparticles induce autophagy and apoptosis via HIF-1α/mTOR signaling in human bronchial epithelial cells.Environmental pollution (Barking, Essex : 1987) · 2023Article
- Developing Benign Ni/g-CIndustrial & engineering chemistry research · 2022Article
- Pulmonary exposure of mice to ammonium perfluoro(2-methyl-3-oxahexanoate) (GenX) suppresses the innate immune response to carbon black nanoparticles and stimulates lung cell proliferation.Inhalation toxicology · 2022Article
- Tuning the Immunostimulation Properties of Cationic Lipid Nanocarriers for Nucleic Acid Delivery.Frontiers in immunology · 2021Article
- Sex differences in the acute and subchronic lung inflammatory responses of mice to nickel nanoparticles.Nanotoxicology · 2020Article
- Carbon Nanotubes and Other Engineered Nanoparticles Induced Pathophysiology on Mesothelial Cells and Mesothelial Membranes.Frontiers in physiology · 2018Review
- Evaluation of uptake and distribution of gold nanoparticles in solid tumors.European physical journal plus · 2015Article
- Pleural mesothelial cells in pleural and lung diseases.Journal of thoracic disease · 2015Review
- Cross regulation between hypoxia-inducible transcription factor-1α (HIF-1α) and transforming growth factor (TGF)-ß1 mediates nickel oxide nanoparticles (NiONPs)-induced pulmonary fibrosis.American journal of translational research · 2015Article
- Spatial relationship quantification between environmental, socioeconomic and health data at different geographic levels.International journal of environmental research and public health · 2014Article
- Wilms' tumor 1 (Wt1) regulates pleural mesothelial cell plasticity and transition into myofibroblasts in idiopathic pulmonary fibrosis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2014Article
- Nickel nanoparticles cause exaggerated lung and airway remodeling in mice lacking the T-box transcription factor, TBX21 (T-bet).Particle and fibre toxicology · 2014Article
- Direct isolation of myofibroblasts and fibroblasts from bleomycin-injured lungs reveals their functional similarities and differences.Fibrogenesis & tissue repair · 2013Article
- Role of hypoxia-inducible factor 1, α subunit and cAMP-response element binding protein 1 in synergistic release of interleukin 8 by prostaglandin E2 and nickel in lung fibroblasts.American journal of respiratory cell and molecular biology · 2013Article
- Nickel-free stainless steel avoids neointima formation following coronary stent implantation.Science and technology of advanced materials · 2012Article
- Innate Immune Responses to Nanoparticle Exposure in the Lung.Journal of environmental immunology and toxicologyArticle
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Pleural diseases (fibrosis and mesothelioma) are a major concern for individuals exposed by inhalation to certain types of particles, metals, and fibers. Increasing attention has focused on the possibility that certain types of engineered nanoparticles (NPs), especially those containing nickel, might also pose a risk for pleural diseases. Platelet-derived growth factor (PDGF) is an important mediator of fibrosis and cancer that has been implicated in the pathogenesis of pleural diseases. In this study, we discovered that PDGF synergistically enhanced nickel NP (NiNP)-induced increases in mRNA and protein levels of the profibrogenic chemokine monocyte chemoattractant protein-1 (MCP-1 or CCL2), and the antifibrogenic IFN-inducible CXC chemokine (CXCL10) in normal rat pleural mesothelial 2 (NRM2) cells in vitro. Carbon black NPs (CBNPs), used as a negative control NP, did not cause a significant increase in CCL2 or CXCL10 in the absence or presence of PDGF. NiNPs prolonged PDGF-induced phosphorylation of the mitogen-activated protein kinase family termed extracellular signal-regulated kinases (ERK)-1 and -2 for up to 24 hours, and NiNPs also synergistically increased PDGF-induced hypoxia-inducible factor (HIF)-1α protein levels in NRM2 cells. Inhibition of ERK-1,2 phosphorylation with the mitogen-activated protein kinase kinase (MEK) inhibitor, PD98059, blocked the synergistic increase in CCL2, CXCL10, and HIF-1α levels induced by PDGF and NiNPs. Moreover, the antioxidant, N-acetyl-L-cysteine (NAC), significantly reduced HIF-1α, ERK-1,2 phosphorylation, and CCL2 protein levels that were synergistically increased by the combination of PDGF and NiNPs. These data indicate that NiNPs enhance the activity of PDGF in regulating chemokine production in NRM2 cells through a mechanism involving reactive oxygen species generation and prolonged activation of ERK-1,2.
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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.