ArticleChemical research in toxicology2010
Reactive oxygen species-activated Akt/ASK1/p38 signaling pathway in nickel compound-induced apoptosis in BEAS 2B cells.
Article in Chemical research in toxicology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.
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Who cites it
62 citing papers in PubMed, 137 citations in OpenAlex.
- Role of the PI3K/AKT signaling pathway in regulating gene expression in rheumatoid arthritis (Review).Molecular medicine reports · 2026Review
- Plant derived tannic acid-based tissue adhesives: From mechanism to advanced design.Acta biomaterialia · 2026Review
- Programmable ROS modulation by nanomedicine for rheumatoid arthritis treatment.Materials today. Bio · 2026Review
- Targeting metalloptosis in tumor therapy: from molecular mechanisms to application of metal nanoparticles.Molecular cancer · 2025Review
- Unveiling the anti-inflammatory potential of RF16, an interleukin 8-derived therapeutic peptide in macrophages.Journal of inflammation (London, England) · 2025Article
- A molecular network analysis and in silico docking of beta-eudesmol, atractylodin and hinesol in patients with advance stage intrahepatic cholangiocarcinoma.Scientific reports · 2025Article
- From ferroptosis to cuproptosis, and calcicoptosis, to find more novel metals-mediated distinct form of regulated cell death.Apoptosis : an international journal on programmed cell death · 2024Review
- Sea food by-products valorization for biomedical applications: evaluation of their wound regeneration capabilities in anFrontiers in veterinary science · 2024Article
- Parkinson's disease models and death signaling: what do we know until now?Frontiers in neuroanatomy · 2024Review
- Oxidative Stress and Redox-Dependent Pathways in Cholangiocarcinoma.Antioxidants (Basel, Switzerland) · 2023Review
- Reactive oxygen species (ROS) scavenging biomaterials for anti-inflammatory diseases: from mechanism to therapy.Journal of hematology & oncology · 2023Review
- Aberrant Akt2 signaling in the RPE may contribute to retinal fibrosis process in diabetic retinopathy.Cell death discovery · 2023Article
- Effectiveness of Albumin-Fused Thioredoxin against 6-Hydroxydopamine-Induced Neurotoxicity In Vitro.International journal of molecular sciences · 2023Article
- Mercury-Induced Oxidative Stress Response in Benthic Foraminifera: An In Vivo Experiment onBiology · 2022Article
- The promising therapeutic potentials of ginsenosides mediated through p38 MAPK signaling inhibition.Heliyon · 2021Review
- p62 functions as a signal hub in metal carcinogenesis.Seminars in cancer biology · 2021Review
- MTA2 silencing attenuates the metastatic potential of cervical cancer cells by inhibiting AP1-mediated MMP12 expression via the ASK1/MEK3/p38/YB1 axis.Cell death & disease · 2021Article
- Manganese Acts upon Insulin/IGF Receptors to Phosphorylate AKT and Increase Glucose Uptake in Huntington's Disease Cells.Molecular neurobiology · 2020Article
- Heavy metals contaminating the environment of a progressive supranuclear palsy cluster induce tau accumulation and cell death in cultured neurons.Scientific reports · 2020Article
- ASK1 Enhances Angiotensin II-Induced Liver FibrosisMediators of inflammation · 2020Article
2 more citing papers are in PubMed but not listed here.
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10 authors at 2 institutions in 2 countries.
Funding
Abstract
Nickel compounds are carcinogenic to humans, possibly through induction of reactive oxygen species (ROS) that damage macromolecules including DNA and proteins. The aim of the present study is to elucidate the role of the ROS-mediated Akt/apoptosis-regulating signal kinase (ASK) 1/p38 pathway in nickel-induced apoptosis. Exposure of human bronchial epithelial cells (BEAS-2B) to nickel compounds induced the generation of ROS and activation of Akt that is associated with the activation of ASK1 and p38 mitogen-activated protein kinase. Immunoblotting suggested a down-regulation of several antiapoptotic proteins, including Bcl-2 and Bcl-xL in the nickel compound-treated cells. Indeed, a notable cell apoptosis following nickel compound treatment is evident as revealed by flow cytometry analysis. N-Acetyl-L-cysteine (NAC, a general antioxidant) and vitamin E or catalase (a specific H(2)O(2) inhibitor) all decreased nickel-induced ROS generation. Scavenging of nickel-induced ROS by NAC or catalase attenuated Akt, ASK1, and p38 MAPK activation and apoptosis, which implies involvement of ROS in the Akt/ASK1/p38 pathway. In addition, nickel-induced activation of p38 MAPK was attenuated by a small interference of RNA specific to ASK1 (siRNA ASK1), implying that p38 MAPK was downstream of ASK1, while ASK1 activation was not reversely regulated by the inhibition of p38 MAPK by SB203580, a widely used p38 MAPK inhibitor. Silencing Akt by siRNA reduced the activation of ASK1 and p38 MAPK and cell apoptosis, whereas without nickel stimulation, siRNA Akt had no effect on the activation of ASK1 and p38 MAPK. Thus, these results suggest that the ROS-dependent Akt-ASK1-p38 axis is important for nickel-induced apoptosis.
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