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Published on: December 10, 2020
Human gingival fibroblasts release high-mobility group box-1 protein through active and passive pathways
K Feghali1, K Iwasaki, K Tanaka
1Section of Periodontology, Department of Hard Tissue Engineering, Graduate School, Tokyo Medical and Dental University, Tokyo 113-8549, Japan.
Periodontal pathogens and cell death increase high-mobility group box-1 (HMGB1) in human gingival fibroblasts. This suggests HMGB1 from fibroblasts contributes to periodontal tissue destruction.
Area of Science:
- Oral biology
- Immunology
- Cell biology
Background:
- High-mobility group box-1 (HMGB1) is a nuclear protein involved in inflammation.
- Extracellular HMGB1 acts as a late mediator of inflammation.
- Human gingival fibroblasts (HGF) are key cells in periodontal tissues.
Purpose of the Study:
- To investigate the effect of periodontal pathogens and cell death on HMGB1 production in HGF.
- To determine if lipopolysaccharides (LPS) from specific bacteria stimulate HMGB1 release.
- To examine the role of apoptosis and necrosis in HMGB1 secretion from HGF.
Main Methods:
- HGF were cultured and stimulated with LPS from Aggregatibacter actinomycetemcomitans, Porphyromonas gingivalis, and Escherichia coli.
- Apoptotic and necrotic cell death were induced in HGF cultures.
- HMGB1 levels in cell supernatants were quantified.
- Immunocytochemistry was used to localize HMGB1 in LPS-stimulated HGF.
Main Results:
- Necrotic and apoptotic HGF released significantly higher amounts of HMGB1.
- LPS from A. actinomycetemcomitans, P. gingivalis, and E. coli induced HMGB1 production in a time-dependent manner.
- HMGB1 translocated from the cytoplasm to the nucleus in LPS-stimulated HGF over time.
Conclusions:
- LPS from periodontal pathogens A. actinomycetemcomitans and P. gingivalis stimulate HMGB1 secretion from HGF.
- Apoptotic and necrotic cell death enhance HMGB1 release from HGF.
- HGF contribute to HMGB1 levels through active secretion and passive release, potentially leading to periodontal tissue destruction.
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