ArticleJournal of leukocyte biology2010
The C-terminal acidic tail is responsible for the inhibitory effects of HMGB1 on efferocytosis.
Article in Journal of leukocyte biology, 2010. 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, 54 citations in OpenAlex.
- Design and synthesis of glycyrrhetinic acid glycosides against acute lung injury and pulmonary fibrosis.Molecular diversity · 2025Article
- Beyond Killing: The Overlooked Contribution of Neutrophils to Tissue Repair.International journal of molecular sciences · 2025Review
- Macrophage‑driven pathogenesis in acute lung injury/acute respiratory disease syndrome: Harnessing natural products for therapeutic interventions (Review).Molecular medicine reports · 2025Review
- Role of the Receptor for Advanced Glycation End Products (RAGE) and Its Ligands in Inflammatory Responses.Biomolecules · 2024Review
- Efferocytosis and Respiratory Disease.International journal of molecular sciences · 2023Review
- Cellular mechanisms underlying the impairment of macrophage efferocytosis.Immunology letters · 2023Review
- Inhaled Pro-Efferocytic Nanozymes Promote Resolution of Acute Lung Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
- Role of necroptosis in airflow limitation in chronic obstructive pulmonary disease: focus on small-airway disease and emphysema.Cell death discovery · 2022Review
- The C-Terminal Acidic Tail Modulates the Anticancer Properties of HMGB1.International journal of molecular sciences · 2022Article
- Intravenous Delivery of Lung-Targeted Nanofibers for Pulmonary Hypertension in Mice.Advanced healthcare materials · 2021Article
- Inflammation Meets Metabolism: Roles for the Receptor for Advanced Glycation End Products Axis in Cardiovascular Disease.Immunometabolism · 2021Article
- Dietary Antioxidants Significantly Attenuate Hyperoxia-Induced Acute Inflammatory Lung Injury by Enhancing Macrophage Function via Reducing the Accumulation of Airway HMGB1.International journal of molecular sciences · 2020Article
- The Neutrophil's Choice: Phagocytose vs Make Neutrophil Extracellular Traps.Frontiers in immunology · 2018Review
- Epigallocatechin-3-gallate attenuates neointimal hyperplasia in a rat model of carotid artery injury by inhibition of high mobility group box 1 expression.Experimental and therapeutic medicine · 2017Article
- HMGB1 Activates Proinflammatory Signaling via TLR5 Leading to Allodynia.Cell reports · 2016Article
- Emerging role of HMGB1 in fibrotic diseases.Journal of cellular and molecular medicine · 2014Review
- HMGB1 in health and disease.Molecular aspects of medicine · 2014Review
- Recent developments in the role of high-mobility group box 1 in systemic lupus erythematosus.Molecular medicine (Cambridge, Mass.) · 2014Review
- Recombinant human interferon alpha 2b prevents and reverses experimental pulmonary hypertension.PloS one · 2014Article
- RAGE is a nucleic acid receptor that promotes inflammatory responses to DNA.The Journal of experimental medicine · 2013Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
HMGB1 was described originally as a nuclear protein involved in DNA binding and transcriptional regulation. However, HMGB1 also has an extracellular role as a potent mediator of inflammation and can diminish the uptake of apoptotic cells by phagocytes, a process called efferocytosis. To explore the mechanism responsible for the ability of HMGB1 to inhibit efferocytosis, we examined the role of the C-terminal acidic tail, a region of HMGB1 that has been shown to participate in specific intramolecular interactions. Deletion of the C-terminal tail abrogated the ability of HMGB1 to decrease murine macrophage ingestion of apoptotic neutrophils and to diminish phagocytosis-induced activation of Erk and Rac-1 in macrophages. We found that RAGE plays a major role in efferocytosis, and deletion of the C-terminal tail of HMGB1 prevented binding of HMGB1 to RAGE but not to other macrophage receptors involved in efferocytosis, such as the α(V)β(3) integrin. Whereas HMGB1 decreased ingestion of apoptotic neutrophils significantly by alveolar macrophages under in vivo conditions in the lungs of mice, this effect was lost when the C-terminal acidic tail was absent from HMGB1. These results demonstrate that the HMGB1 C-terminal tail is responsible for the inhibitory effects of HMGB1 on phagocytosis of apoptotic neutrophils under in vitro and in vivo conditions.
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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.