ArticleParticle and fibre toxicology2012
Multi-walled carbon nanotubes induce COX-2 and iNOS expression via MAP kinase-dependent and -independent mechanisms in mouse RAW264.7 macrophages.
Article in Particle and fibre toxicology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 102 citations in OpenAlex.
- Role of the protease-activated receptor 2 in multi-walled carbon nanotube-induced macrophage polarizationFrontiers in toxicology · 2026Article
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- Do Carbon Nanotubes and Asbestos Fibers Exhibit Common Toxicity Mechanisms?Nanomaterials (Basel, Switzerland) · 2022Review
- Acupoint Catgut-Embedding Therapy Inhibits NF-BioMed research international · 2022Article
- Auraptene, a Monoterpene Coumarin, Inhibits LTA-Induced Inflammatory Mediators via Modulating NF-Evidence-based complementary and alternative medicine : eCAM · 2021Article
- Carbon Black Nanoparticles Selectively Alter Follicle-Stimulating Hormone ExpressionFrontiers in neuroscience · 2021Article
- Combined Toxicity of Metal Nanoparticles: Comparison of Individual and Mixture Particles Effect.Advances in experimental medicine and biology · 2021Article
- Comparative analysis of lung and blood transcriptomes in mice exposed to multi-walled carbon nanotubes.Toxicology and applied pharmacology · 2020Article
- Signaling Pathways Implicated in Carbon Nanotube-Induced Lung Inflammation.Frontiers in immunology · 2020Review
- Resolution of Pulmonary Inflammation Induced by Carbon Nanotubes and Fullerenes in Mice: Role of Macrophage Polarization.Frontiers in immunology · 2020Article
- Identification of β-carboline and canthinone alkaloids as anti-inflammatory agents but with different inhibitory profile on the expression of iNOS and COX-2 in lipopolysaccharide-activated RAW 264.7 macrophages.Journal of natural medicines · 2019Article
- sTLR4/sMD-2 complex alleviates LPS-induced acute lung injury by inhibiting pro-inflammatory cytokines and chemokine CXCL1 expression.Experimental and therapeutic medicine · 2018Article
- The effects of subacute inhaled multi-walled carbon nanotube exposure on signaling pathways associated with cholesterol transport and inflammatory markers in the vasculature of wild-type mice.Toxicology letters · 2018Article
- Targeting myeloid regulators by paclitaxel-loaded enzymatically degradable nanocups.Nanoscale · 2018Article
- TIMP1 promotes multi-walled carbon nanotube-induced lung fibrosis by stimulating fibroblast activation and proliferation.Nanotoxicology · 2017Article
- Quantitative analysis of the role of fiber length on phagocytosis and inflammatory response by alveolar macrophages.Biochimica et biophysica acta. General subjects · 2017Article
- Atomic layer deposition coating of carbon nanotubes with zinc oxide causes acute phase immune responses in human monocytes in vitro and in mice after pulmonary exposure.Particle and fibre toxicology · 2016Article
- MCPIP1 Regulates Alveolar Macrophage Apoptosis and Pulmonary Fibroblast Activation After in vitro Exposure to Silica.Toxicological sciences : an official journal of the Society of Toxicology · 2016Article
- Integrated Analysis of Dysregulated ncRNA and mRNA Expression Profiles in Humans Exposed to Carbon Nanotubes.PloS one · 2016Article
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundCarbon nanotubes (CNTs) are engineered graphene cylinders with numerous applications in engineering, electronics and medicine. However, CNTs cause inflammation and fibrosis in the rodent lung, suggesting a potential human health risk. We hypothesized that multi-walled CNTs (MWCNTs) induce two key inflammatory enzymes in macrophages, cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS), through activation of extracellular signal-regulated kinases (ERK1,2).
methodsRAW264.7 macrophages were exposed to MWCNTs or carbon black nanoparticles (CBNPs) over a range of doses and time course. Uptake and subcellular localization of MWCNTs was visualized by transmission electron microscopy (TEM). Protein levels of COX-2, iNOS, and ERK1,2 (total ERK and phosphorylated ERK) were measured by Western blot analysis. Prostaglandin-E(2) (PGE(2)) and nitric oxide (NO) levels in cell supernatants were measured by ELISA and Greiss assay, respectively.
resultsMWCNTs, but not CBNPs, induced COX-2 and iNOS in a time- and dose-dependent manner. COX-2 and iNOS induction by MWCNTs correlated with increased PGE(2) and NO production, respectively. MWCNTs caused ERK1,2 activation and inhibition of ERK1,2 (U0126) blocked MWCNT induction of COX-2 and PGE2 production, but did not reduce the induction of iNOS. Inhibition of iNOS (L-NAME) did not affect ERK1,2 activation, nor did L-NAME significantly decrease COX-2 induction by MWCNT. Nickel nanoparticles (NiNPs), which are present in MWCNTs as a residual catalyst, also induced COX-2 via ERK-1,2. However, a comparison of COX-2 induction by MWCNTs containing 4.5 and 1.8% Ni did not show a significant difference in ability to induce COX-2, indicating that characteristics of MWCNTs in addition to Ni content contribute to COX-2 induction.
conclusionThis study identifies COX-2 and subsequent PGE(2) production, along with iNOS induction and NO production, as inflammatory mediators involved in the macrophage response to MWCNTs. Furthermore, our work demonstrates that COX-2 induction by MWCNTs in RAW264.7 macrophages is ERK1,2-dependent, while iNOS induction by MWCNTs is ERK1,2-independent. Our data also suggest contributory physicochemical factors other than residual Ni catalyst play a role in COX-2 induction to MWCNT.
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