ArticlePloS one2012
Dengue virus infection mediates HMGB1 release from monocytes involving PCAF acetylase complex and induces vascular leakage in endothelial cells.
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 42 papers.
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Who cites it
42 citing papers in PubMed, 82 citations in OpenAlex.
- A Retrospective Analysis of the Significance of Haemoglobin SS and SC in Disease Outcome in Patients With Sickle Cell Disease and Dengue Fever.EBioMedicine · 2015Trial
- Abdominal Symptoms During the Febrile Phase Indicate Profound Innate Immune Responses in Dengue.Biology · 2026Article
- Reduced dengue virus pre-membrane protein-HMGB1 interaction activates host cell transcription to attenuate infection.NPJ vaccines · 2026Article
- Low-density granulocytes and neutrophil extracellular traps in dengue, impacts of interferon alpha and cell-free DNA.Scientific reports · 2025Article
- Article
- Review
- High-mobility group box 1 (HMGB1) in COVID-19: extrapolation of dangerous liaisons.Inflammopharmacology · 2022Review
- MicroRNA 573 Rescues Endothelial Dysfunction during Dengue Virus Infection under PPARγ Regulation.Journal of virology · 2022Article
- Possible roles of anti-type II collagen antibody and innate immunity in the development and progression of diabetic retinopathy.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2022Review
- Intracellular translocation of HMGB1 is important for Zika virus replication in Huh7 cells.Scientific reports · 2022Article
- Elevated TNF-α Induces Thrombophagocytosis by Mononuclear Cells in ex vivo Whole-Blood Co-Culture with Dengue Virus.Journal of inflammation research · 2022Article
- Article
- Pathogen-induced inflammation is attenuated by the iminosugar MON-DNJ via modulation of the unfolded protein response.Immunology · 2021Article
- Article
- Melatonin may decrease risk for and aid treatment of COVID-19 and other RNA viral infections.Open heart · 2021Article
- Antiviral Role of Phenolic Compounds against Dengue Virus: A Review.Biomolecules · 2020Review
- Sirtuin 1-dependent regulation of high mobility box 1 in hypoxia-reoxygenated brain microvascular endothelial cells: roles in neuronal amyloidogenesis.Cell death & disease · 2020Article
- Sphingosine kinase 1 regulates HMGB1 translocation by directly interacting with calcium/calmodulin protein kinase II-δ in sepsis-associated liver injury.Cell death & disease · 2020Article
- Cystitis-Related Bladder Pain Involves ATP-Dependent HMGB1 Release from Macrophages and Its Downstream HCells · 2020Article
- High-Mobility Group Box 1 Protein Signaling in Painful Diabetic Neuropathy.International journal of molecular sciences · 2020Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
High mobility group box 1 (HMGB1) protein is released from cells as a pro-inflammatory cytokine in response to an injury or infection. During dengue hemorrhagic fever (DHF)/dengue shock syndrome (DSS), a number of pro-inflammatory cytokines are released, contributing to disease pathogenesis. In this study, the release of HMGB1 from human myelogenous leukemia cell line K562 and primary peripheral blood monocytes (PBM) cells was examined during dengue virus (DV)-infection. HMGB1 was shown to translocate from cell nuclei to the cytoplasm in both K562- and PBM-infected cells. The translocation of HMGB1 from the nucleus to the cytoplasm was shown to be mediated by the host cell p300/CBP-associated factor (PCAF) acetylase complex in K562 cells. In addition, DV capsid protein was observed to be the putative viral protein in actuating HMGB1 migration from the nucleus to cytoplasm through the involvement of PCAF acetylase. HMGB1 was released from DV-infected K562 cells into the extracellular milieu in a multiplicity of infection (M.O.I.)-independent manner and its release can be inhibited by the addition of 1-5 mM of ethyl pyruvate (EP) in a dose-dependent manner. Application of DV-infected K562 cell culture supernatants to primary endothelial cells induced vascular permeability. In contrast, supernatants from DV-infected K562 cells treated with EP or HMGB1 neutralizing antibody were observed to maintain the structural integrity of the vascular barrier.
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