ArticleJournal of cellular physiology2016
Translocation of Endogenous Danger Signal HMGB1 From Nucleus to Membrane Microvesicles in Macrophages.
Article in Journal of cellular physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
What it found
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Who cites it
33 citing papers in PubMed, 61 citations in OpenAlex.
- Influence of hemoadsorption during cardiopulmonary bypass on blood vesicle count and function.Journal of translational medicine · 2020Trial
- Taxane chemotherapy promotes response to TIM-3 checkpoint blockade via STING-mediated ER stress and HMGB1 secretion.Cell reports. Medicine · 2026Article
- Novel perspectives on extracellular vesicles in autoimmune diseases: immunogenicity, inflammation, and immune surveillance.The Journal of clinical investigation · 2026Review
- Ashes to Rashes: An Exploration of the Intersection Between Smoking and Cutaneous Lupus Erythematosus.Biomolecules · 2025Review
- Virus and cell specific HMGB1 secretion and subepithelial infiltrate formation in adenovirus keratitis.PLoS pathogens · 2025Article
- Circulating extracellular vesicles as novel biomarkers for pulmonary arterial hypertension in patients with systemic lupus erythematosus.Frontiers in immunology · 2024Article
- Vesicular HMGB1 release from neurons stressed with spreading depolarization enables confined inflammatory signaling to astrocytes.Journal of neuroinflammation · 2023Article
- Bioengineered extracellular vesicles: future of precision medicine for sepsis.Intensive care medicine experimental · 2023Review
- Targeting Persistent Changes in Neuroimmune and Epigenetic Signaling in Adolescent Drinking to Treat Alcohol Use Disorder in Adulthood.Pharmacological reviews · 2023Review
- The impact of environmental contaminants on extracellular vesicles and their key molecular regulators: A literature and database-driven review.Environmental and molecular mutagenesis · 2023Review
- The role of HMGB1/RAGE/TLR4 signaling pathways in cigarette smoke-induced inflammation in chronic obstructive pulmonary disease.Immunity, inflammation and disease · 2022Review
- Environmental Exposures and Extracellular Vesicles: Indicators of Systemic Effects and Human Disease.Current environmental health reports · 2022Review
- CD47 interactions with exportin-1 limit the targeting of mJournal of cell communication and signaling · 2022Article
- Emerging Insights into the Impact of Air Pollution on Immune-Mediated Asthma Pathogenesis.Current allergy and asthma reports · 2022Review
- The mechanism of HMGB1 secretion and release.Experimental & molecular medicine · 2022Review
- Extracellular Vesicles, New Players in Sepsis and Acute Respiratory Distress Syndrome.Frontiers in cellular and infection microbiology · 2022Review
- Applications, challenges and prospects of mesenchymal stem cell exosomes in regenerative medicine.Stem cell research & therapy · 2021Article
- Extracellular Vesicles: A Double-Edged Sword in Sepsis.Pharmaceuticals (Basel, Switzerland) · 2021Review
- Recent advances in Extracellular Vesicles and their involvements in vasculitis.Free radical biology & medicine · 2021Review
- Extracellular vesicles and lupus nephritis - New insights into pathophysiology and clinical implications.Journal of autoimmunity · 2020Review
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 3 countries.
Funding
Abstract
High mobility group box 1 (HMGB1) is a nuclear protein that can be released from activated or dead cells. Extracellular HMGB1 can serve as a "danger signal" and novel cytokine that mediates sterile inflammation. In addition to its soluble form, extracellular HMGB1 can also be carried by membrane microvesicles. However, the cellular mechanisms responsible for nuclear HMGB1 translocation to the plasma membrane and release onto membrane microvesicles have not been investigated. Tobacco smoking is a major cause of sterile inflammation in many diseases. Smoking also increases blood levels of HMGB1. In this study, we found that exposure of macrophages to tobacco smoke extract (TSE) stimulated HMGB1 expression, redistribution, and release into the extracellular milieu both as a soluble molecule and, surprisingly, as a microvesicle-associated form (TSE-MV). Inhibition of chromosome region maintenance-1 (CRM1), a nuclear exporter, attenuated TSE-induced HMGB1 redistribution from the nucleus to the cytoplasm, and then its release on TSE-MVs. Our study demonstrates a novel mechanism for the translocation of nuclear HMGB1 to the plasma membrane, and then its release in a microvesicle-associated form. J. Cell. Physiol. 231: 2319-2326, 2016. © 2016 Wiley Periodicals, Inc.
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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.