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The Relationship between Apoptosis and High-Mobility Group Protein 1 Release from Murine Macrophages Stimulated with Lipopolysaccharide or Polyinosinic-Polycytidylic Acid
Abstract
High-mobility group protein 1 (HMGB1) is a nonhistone nuclear protein whose function depends on cellular location. Inside the cell, HMGB1 modulates a variety of important cellular processes, including transcription, whereas outside the cell, HMGB1 acts as a cytokine that can promote inflammation and mediate sepsis and arthritis in animal models. In in vitro studies, proinflammatory molecules such as LPS, lipoteichoic acid, polyinosinic-polycytidylic acid (poly(I:C)), TNF-α, and type I and II IFNs can induce HMGB1 release from macrophages. Although these agents can activate cells, they can also induce apoptosis under certain circumstances. Therefore, because of evidence that apoptotic as well as necrotic cells can contribute to HMGB1-mediated events in sepsis, we have investigated the relationship between apoptosis and HMGB1 release in macrophages and other cells. In these experiments, using RAW 264.7 cells as a model, LPS and poly(I:C) caused HMGB1 release into the medium whereas CpG ODN failed to induce this response. With both LPS and poly(I:C), the extent of HMGB1 release correlated with the occurrence of apoptosis as measured by caspase 3 activation, lactate dehydrogenase release, and TUNEL staining. Similar results were obtained with primary murine macrophages as well as human Jurkat T cells. For Jurkat cells, poly(I:C) and NO donors induced apoptosis as well as HMGB1 release. Together, these results indicate that HMGB1 release from macrophages is correlated with the occurrence of apoptosis and suggest that these processes reflect common mechanisms and can occur concomitantly.
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“Although it was initially thought that HMGB1 is released only from the nucleus during primary necrosis, recent data indicate that HMGB1 can be released during secondary necrosis following apoptosis 27,48–50.”
From Immunogenic and tolerogenic cell death (2009) · cites this paper as [50]
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Metadata
- Authors
- Jiang, W., Bell, C. W., & Pisetsky, D. S.
- Affiliations
- Duke University (US)
- Corresponding author
- Jiang, Weiwen
- ORCID
- Pisetsky, David S
- Venue
- The Journal of Immunology
- Publisher
- Oxford University Press (OUP)
- Published
- 2007-05
- Volume
- 178
- Issue
- 10
- Pages
- 6495-6503
- ISSN
- 0022-1767 (ISSN-L)
- 1550-6606
- OpenAlex
- W2130822772
- Cited by
- 134
- References
- 45
- Citations by year
- 2025: 2 · 2024: 1 · 2023: 6 · 2022: 5 · 2021: 4 · 2020: 3 · 2019: 4 · 2018: 4 · 2017: 8 · 2016: 6 · 2015: 7 · 2014: 5 · 2013: 10 · 2012: 9
- FWCI
- 10.26
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- The Journal of Immunology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute of Allergy and Infectious Diseases (AI44808)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Clinical Biochemistry › Advanced Glycation End Products research
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Keywords
- HMGB1, apoptosis, macrophages, lipopolysaccharide, poly(I:C), CpG oligodeoxynucleotides, caspase-3, necrosis, sepsis, inflammation, Jurkat cells, RAW 264.7 macrophages, nitric oxide donors, HMGB1 release
- MeSH terms
- Animals, Cell Line, Extracellular Space, Female, Humans, Lipopolysaccharides, Macrophage Activation, Mice, Inbred BALB C, Oligodeoxyribonucleotides, Poly I-C, Apoptosis, Macrophages, Peritoneal, Jurkat Cells, Protein Transport, HMGB1 Protein, Toll-Like Receptors, Mice
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