ArticlePloS one2012
High-mobility group box-1 induces proinflammatory cytokines production of Kupffer cells through TLRs-dependent signaling pathway after burn injury.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 60 citations in OpenAlex.
- High mobility group box protein 1 sensitizes mononuclear cells to further contact with lipopolysaccharide.Central-European journal of immunology · 2024Article
- Regulation of Key Immune-Related Genes in the Heart Following Burn Injury.Journal of personalized medicine · 2022Article
- Plasma extracellular vesicles released after severe burn injury modulate macrophage phenotype and function.Journal of leukocyte biology · 2022Article
- Burn Injury Induces Proinflammatory Plasma Extracellular Vesicles That Associate with Length of Hospital Stay in Women: CRP and SAA1 as Potential Prognostic Indicators.International journal of molecular sciences · 2021Article
- Absence of Stress Hyperglycemia Indicates the Most Severe Form of Blunt Liver Trauma.Diagnostics (Basel, Switzerland) · 2021Article
- Disulfide High-Mobility Group Box 1 Drives Ischemia-Reperfusion Injury in Human Liver Transplantation.Hepatology (Baltimore, Md.) · 2021Article
- Hepatic inflammation after burn injury is associated with necroptotic cell death signaling.The journal of trauma and acute care surgery · 2020Article
- Negative Regulation of Tec Kinase Alleviates LPS-Induced Acute Kidney Injury in Mice via theTLR4/NF-BioMed research international · 2020Article
- Suppression of Cisplatin-Induced Hepatic Injury in Rats Through Alarmin High-Mobility Group Box-1 Pathway byDrug design, development and therapy · 2020Article
- p38MAPK plays a pivotal role in the development of acute respiratory distress syndrome.Clinics (Sao Paulo, Brazil) · 2019Review
- Electroacupuncture Alleviates Spared Nerve Injury-Induced Neuropathic Pain And Modulates HMGB1/NF-κB Signaling Pathway In The Spinal Cord.Journal of pain research · 2019Article
- Inhibitory effects of miR-25 targeting HMGB1 on macrophage secretion of inflammatory cytokines in sepsis.Oncology letters · 2018Article
- High-Mobility Group Box-1 and Liver Disease.Hepatology communications · 2018Review
- HMGB1 Increases IL-1β Production in Vascular Smooth Muscle Cells via NLRP3 Inflammasome.Frontiers in physiology · 2018Article
- Toll-Like Receptor Signaling in Burn Wound Healing and Scarring.Advances in wound care · 2017Review
- The liver is a metabolic and immunologic organ: A reconsideration of metabolic decompensation due to infection in inborn errors of metabolism (IEM).Molecular genetics and metabolism · 2017Review
- Inhibitor of Tec kinase, LFM-A13, decreases pro-inflammatory mediators production in LPS-stimulated RAW264.7 macrophages via NF-κB pathway.Oncotarget · 2017Article
- Damage-associated molecular patterns (DAMPs) released after burn are associated with inflammation and monocyte activation.Burns : journal of the International Society for Burn Injuries · 2017Article
- High-Mobility Group Box 1 (HMGB1) Is Elevated Systemically in Persons with Acute or Chronic Traumatic Spinal Cord Injury.Journal of neurotrauma · 2017Article
- HMGB1 translocation and release mediate cigarette smoke-induced pulmonary inflammation in mice through a TLR4/MyD88-dependent signaling pathway.Molecular biology of the cell · 2017Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Kupffer cells (KCs) were a significant source of cytokine release during the early stage of severe burns. High mobility group box protein 1 (HMGB1) was recently identified as a new type of proinflammatory cytokine. The ability of HMGB1 to generate inflammatory responses after burn trauma has not been well characterized. KCs were isolated from sham animals and rats with a 30% full-thickness burn, and then were stimulated with increasing concentrations of HMGB1. The levels of Tumor necrosis factor (TNF)-α and interleukin (IL)-1β in culture supernatant were measured by enzyme-linked immunosorbent assay. Northern blot analysis was performed to detect the expressions of TNF-α and IL-1β mRNAs. The activities of p38 MAPK and JNK (by Western blot analysis) as well as NF-κB (by EMSA) in KCs were also examined. As a result, HMGB1 in vitro upregulated expressions of TNF-α and IL-1β of KCs in a dose-dependent manner, and HMGB1 promoted KCs from burn rats to produce significantly more TNF-α and IL-1β proteins than those from sham animals. After harvested from burn rats, KCs were pre-incubated with anti-TLR2 or anti-TLR4 antibody prior to HMGB1 administration. HMGB1 exposure not only significantly increased expressions of TNF-α and IL-1β mRNAs in KCs from burn rats, but also enhanced activities of p38 MAPK, JNK and NF-κB. However, these upregulation events were all reduced by pre-incubation with anti-TLR2 or anti-TLR4 antibody. These results indicate that HMGB1 induces proinflammatory cytokines production of KCs after sever burn injury, and this process might be largely dependent on TLRs-dependent MAPKs/NF-κB signal pathway.
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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.