ArticleToxicology and applied pharmacology2013
Unfolded protein response (UPR) signaling regulates arsenic trioxide-mediated macrophage innate immune function disruption.
Article in Toxicology and applied pharmacology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 62 citations in OpenAlex.
- Epigallocatechin-3-gallate as a hepatoprotective agent against ochratoxin a: modulating ER stress and NF-κB/TNF-α/IL-6 responses.Mycotoxin research · 2026Article
- Common molecular profile of multiple structurally distinct warfare arsenicals in causing cutaneous chemical vesicant injury.Scientific reports · 2025Article
- Mechanistic understanding of the toxic effects of arsenic and warfare arsenicals on human health and environment.Cell biology and toxicology · 2023Review
- The genomic landscape of sensitivity to arsenic trioxide uncovered by genome-wide CRISPR-Cas9 screening.Frontiers in oncology · 2023Article
- Arsenic and Human Health: Genotoxicity, Epigenomic Effects, and Cancer Signaling.Biological trace element research · 2022Review
- Connections between endoplasmic reticulum stress-associated unfolded protein response, mitochondria, and autophagy in arsenic-induced carcinogenesis.Seminars in cancer biology · 2021Review
- Recruitment of endoplasmic reticulum-targeted and cytosolic mRNAs into membrane-associated stress granules.RNA (New York, N.Y.) · 2021Article
- Protective role of HO-1 against acute kidney injury caused by cutaneous exposure to arsenicals.Annals of the New York Academy of Sciences · 2020Article
- Arsenic Exposure and Compromised Protein Quality Control.Chemical research in toxicology · 2020Review
- Old dog, new trick: Trivalent arsenic as an immunomodulatory drug.British journal of pharmacology · 2020Review
- Endoplasmic Reticulum Stress Pathway, the Unfolded Protein Response, Modulates Immune Function in the Tumor Microenvironment to Impact Tumor Progression and Therapeutic Response.International journal of molecular sciences · 2019Review
- Transcriptome-wide analysis of changes in the fetal placenta associated with prenatal arsenic exposure in the New Hampshire Birth Cohort Study.Environmental health : a global access science source · 2019Article
- Article
- Chronic low dose arsenic exposure preferentially perturbs mitotic phase of the cell cycle.Genes & cancer · 2019Article
- Ameliorative effects of selenium on the excess apoptosis of the jejunum caused by AFBToxicology research · 2018Article
- Phosgene oxime: Injury and associated mechanisms compared to vesicating agents sulfur mustard and lewisite.Toxicology letters · 2018Review
- Double-Sided Personality: Effects of Arsenic Trioxide on Inflammation.Inflammation · 2018Review
- Metabolism, toxicity and anticancer activities of arsenic compounds.Oncotarget · 2017Review
- ATF4 regulates arsenic trioxide-mediated NADPH oxidase, ER-mitochondrial crosstalk and apoptosis.Archives of biochemistry and biophysics · 2016Article
- Defining cutaneous molecular pathobiology of arsenicals using phenylarsine oxide as a prototype.Scientific reports · 2016Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
Arsenic exposure is known to disrupt innate immune functions in humans and in experimental animals. In this study, we provide a mechanism by which arsenic trioxide (ATO) disrupts macrophage functions. ATO treatment of murine macrophage cells diminished internalization of FITC-labeled latex beads, impaired clearance of phagocytosed fluorescent bacteria and reduced secretion of pro-inflammatory cytokines. These impairments in macrophage functions are associated with ATO-induced unfolded protein response (UPR) signaling pathway characterized by the enhancement in proteins such as GRP78, p-PERK, p-eIF2α, ATF4 and CHOP. The expression of these proteins is altered both at transcriptional and translational levels. Pretreatment with chemical chaperon, 4-phenylbutyric acid (PBA) attenuated the ATO-induced activation in UPR signaling and afforded protection against ATO-induced disruption of macrophage functions. This treatment also reduced ATO-mediated reactive oxygen species (ROS) generation. Interestingly, treatment with antioxidant N-acetylcysteine (NAC) prior to ATO exposure, not only reduced ROS production and UPR signaling but also improved macrophage functions. These data demonstrate that UPR signaling and ROS generation are interdependent and are involved in the arsenic-induced pathobiology of macrophage. These data also provide a novel strategy to block the ATO-dependent impairment in innate immune responses.
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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.