ArticleRedox biology2019
Extracellular vesicle-mediated macrophage activation: An insight into the mechanism of thioredoxin-mediated immune activation.
Article in Redox biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 26 citations in OpenAlex.
- Review
- Extracellular Vesicle Properties and Functions Are Defined by the Originating Cell's Fitness Status.Journal of extracellular biology · 2026Article
- Lipidomic Analysis of Plasma Extracellular Vesicles from Adiponectin Deficient Mice or Metabolic Syndrome Patients Reveals Pro-Oxidative and Pro-Inflammatory Lipid Signatures Correlating with Metabolic Dysfunction.Journal of extracellular vesicles · 2026Article
- Mitochondrial cargo quality determines the paracrine effects of extracellular vesicles derived from vascular endothelial cells.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2025Article
- GAPDH-Silence Microsphere via Reprogramming Macrophage Metabolism and eradicating Bacteria for Diabetic infection bone regeneration.Journal of nanobiotechnology · 2024Article
- Thioredoxin1 Binding Metastasis-Associated Lung Adenocarcinoma Transcript 1 Attenuates Inflammation and Apoptosis after Intracerebral Hemorrhage.Aging and disease · 2024Article
- Electrochemical detection of extracellular vesicles for early diagnosis: a focus on disease biomarker analysis.Extracellular vesicles and circulating nucleic acids · 2024Review
- Extracellular Vesicles Released after Doxorubicin Treatment in Rats Protect Cardiomyocytes from Oxidative Damage and Induce Pro-Inflammatory Gene Expression in Macrophages.International journal of molecular sciences · 2022Article
- Anthracycline-induced cardiotoxicity and cell senescence: new therapeutic option?Cellular and molecular life sciences : CMLS · 2022Review
- The RelB-BLNK Axis Determines Cellular Response to a Novel Redox-Active Agent Betamethasone during Radiation Therapy in Prostate Cancer.International journal of molecular sciences · 2022Article
- Extracellular vesicles mediated proinflammatory macrophage phenotype induced by radiotherapy in cervical cancer.BMC cancer · 2022Article
- A Redox-active Mn Porphyrin, MnTnBuOE-2-PyPOxidative medicine and cellular longevity · 2022Article
- Extracellular Vesicles in Innate Immune Cell Programming.Biomedicines · 2021Review
- Osteocrin attenuates inflammation, oxidative stress, apoptosis, and cardiac dysfunction in doxorubicin-induced cardiotoxicity.Clinical and translational medicine · 2020Article
- Article
- Cardioprotective Role of Melatonin in Acute Myocardial Infarction.Frontiers in physiology · 2020Review
- Chemical Effect of Bisphenol A on Non-Alcoholic Fatty Liver Disease.International journal of environmental research and public health · 2019Review
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
Extracellular vesicles (EVs) generated from redox active anticancer drugs are released into the extracellular environment. These EVs contain oxidized molecules and trigger inflammatory responses by macrophages. Using a mouse model of doxorubicin (DOX)-induced tissue injury, we previously found that the major sources of circulating EVs are from heart and liver, organs that are differentially affected by DOX. Here, we investigated the effects of EVs from cardiomyocytes and those from hepatocytes on macrophage activation. EVs from H9c2 rat cardiomyocytes (H9c2 EVs) and EVs from FL83b mouse hepatocytes (FL83 b EVs) have different levels of protein-bound 4-hydroxynonenal and thus different immunostimulatory effects on mouse RAW264.7 macrophages. H9c2 EVs but not FL83 b EVs induced both pro-inflammatory and anti-inflammatory macrophage activation, mediated by NFκB and Nrf-2 pathways, respectively. DOX enhanced the effects of H9c2 EVs but not FL83 b EVs. While EVs from DOX-treated H9c2 cells (H9c2 DOXEVs) suppressed mitochondrial respiration and increased glycolysis of macrophages, EVs from DOX-treated FL83b cells (FL83b DOXEVs) enhanced mitochondrial reserve capacity. Mechanistically, the different immunostimulatory functions of H9c2 EVs and FL83 b EVs are regulated, in part, by the redox status of the cytoplasmic thioredoxin 1 (Trx1) of macrophages. H9c2 DOXEVs lowered the level of reduced Trx1 in cytoplasm while FL83b DOXEVs did the opposite. Trx1 overexpression alleviated the effect of H9c2 DOXEVs on NFκB and Nrf-2 activation and prevented the upregulation of their target genes. Our findings identify EVs as a novel Trx1-mediated redox mediator of immune response, which greatly enhances our understanding of innate immune responses during cancer therapy.
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