Histone-deacetylase-inhibitory effects of periodontopathic-bacterial metabolites induce human gingival epithelial Ca9-22 cell death

Uemichi, Kazuki; Mikami, Yohei; Watanabe, Takayasu; Shinozuka, Keiji; Tonogi, Morio; Tsuda, Hiromasa

doi:10.1007/s10266-022-00775-9

Cited by 3 publications

(10 citation statements)

References 24 publications

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“…Residual cells were collected and lysed in lysis buffer, and the lysates were used for western blot to confirm the ATG5 reduction. Transfected cells were treated with 5 mM sodium butyrate or 10 mM sodium propionate in 1% FBS RPMI1640 for 48 h. Cell death assays using SYTOX-Green dye were performed as previously described [3,6].…”

Section: Atg5 Knockdown and Sytox-green Cell Death Assaymentioning

confidence: 99%

“…It has been demonstrated that sodium butyrate treatment of Ca9-22 cells altered the expression of many autophagy-and ROS generation-related genes [6]. Therefore, whether Ca9-22 cells release ROS by treatment with sodium butyrate or sodium propionate was examined.…”

Section: Sodium Butyrate or Sodium Propionate-treated Ca9-22 Cells Ge...mentioning

confidence: 99%

“…These events consistently demonstrate the importance of autophagy induction in butyrate-induced cell death. In contrast, Uemichi et al demonstrated that butyrate or propionate induces histone H3 acetylation by their histone deacetylase inhibitory activities, and the effects are important for SCFA-dependent death of Ca9-22 cells [6]. Although several factors associated with butyrate-induced cell death have been reported, the relationship between these factors is unclear.…”

Section: Introductionmentioning

confidence: 96%

“…Although several factors associated with butyrate-induced cell death have been reported, the relationship between these factors is unclear. Because gene expressions related to autophagy induction and reactive oxygen species (ROS) production are upregulated during butyrate treatment [6], the relationship between autophagy induction and ROS generation during SCFA-induced cell death and subsequent release of damage-associated molecular patterns (DAMPs) was investigated. The potential methods for prevention of periodontal disease were additionally discussed.…”

Section: Introductionmentioning

confidence: 99%

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Reactive oxygen species generation required for autophagy induction during butyrate- or propionate-induced release of damage-associated molecular patterns from dying gingival epithelial Ca9-22 cells

Miyake,

Mikami,

Asayama

et al. 2024

J Oral Sci

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Purpose: Bacterial cells in mature dental plaque produce a high concentration of short-chain fatty acids (SCFAs) such as butyrate and propionate. SCFA-treatment on human gingival epithelial Ca9-22 cells induced cell death. However, the exact mechanism underlying cell death remains unclear. In this study, the relationship between reactive oxygen species (ROS) and autophagy induction during SCFA-induced cell death was examined. Methods: Human gingival epithelial Ca9-22 cells were treated with butyrate or propionate to induce cell death and the number of dead cells were measured using SYTOX-green dye. A siRNA for ATG5 and N-acetylcysteine (NAC) were used for autophagy reduction and ROS-scavenging, respectively. Release of damage-associated molecular patterns (DAMPs) such as Sin3A-associated protein 130 (SAP130) and high-mobility group box 1 (HMGB1) were detected using western blot. Results: Reducing autophagy significantly suppressed SCFA-induced Ca9-22 cell death. ROS generation was observed upon SCFA treatment, and scavenging ROS with NAC decreased cell death. NAC also reduced the SCFA-induced increase in microtubule-associated protein 1 light chain 3B (LC3B)-I and LC3B-II, and mitigated the release of DAMPs. Conclusion:The findings suggest that ROS generation is necessary for autophagy, which is required for SCFA-induced cell death and accompanying DAMP release.

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Section: Atg5 Knockdown and Sytox-green Cell Death Assaymentioning

confidence: 99%

Section: Sodium Butyrate or Sodium Propionate-treated Ca9-22 Cells Ge...mentioning

confidence: 99%

Section: Introductionmentioning

confidence: 96%

Section: Introductionmentioning

confidence: 99%

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Reactive oxygen species generation required for autophagy induction during butyrate- or propionate-induced release of damage-associated molecular patterns from dying gingival epithelial Ca9-22 cells

Miyake,

Mikami,

Asayama

et al. 2024

J Oral Sci

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“…Ca9-22 cells were used as representative gingival epithelial cell [19][20][21] purchased from JCRB Cell Bank (Tokyo, Japan; ID: JCRB0625). Ca9-22 cells were cultured in Dulbecco's modified Eagle's medium (Wako Pure Chemical Industries, Osaka, Japan) containing 10% fetal bovine serum (Biowest, Nuaillé, France), 100 μg/mL penicillin, 100 μg/mL streptomycin, and 2 mM L-glutamine (Wako Pure Chemical Industries).…”

Section: Cell Culturementioning

confidence: 99%

P38α contributes to TNF‐α‐induced IL‐8 production in human gingival cells

et al. 2023

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Tumor necrosis factor‐alpha (TNF‐α) is a major inflammatory cytokine that induces interleukin (IL)‐8 production. Although some studies have reported the involvement of the p38 MAPK signaling pathway in TNF‐α‐induced IL‐8 production, its specific regulatory mechanisms in gingival epithelial cells (GECs) are still poorly understood. In the present study, Ca9‐22 cells were used as representative GECs to investigate the effect of p38 signaling on TNF‐α‐induced IL‐8 production. We found that TNF‐α enhanced IL‐8 production in Ca9‐22 cells by activating the p38 signaling pathway, and one of its isoforms, p38α, played a key role. P38α deletion markedly inhibited TNF‐α‐induced IL‐8 expression in Ca9‐22 cells, while p38α gene rescue could reverse this effect. Further studies revealed that TNF‐α‐induced IL‐8 production was markedly reduced when the threonine 180 and tyrosine 182 p38α phosphorylation sites were targeted for mutagenesis to alanine and phenylalanine, respectively, suggesting their critical role in the process. In conclusion, p38α plays an important role in TNF‐α‐induced IL‐8 production, providing a potential therapeutic target to prevent and treat periodontal disease.

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Role of the nucleotide-binding oligomerization domain-containing protein 1 pathway in the development of periodontitis

Mao,

Inoue,

Goda

2024

Journal of Oral Biosciences

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Histone-deacetylase-inhibitory effects of periodontopathic-bacterial metabolites induce human gingival epithelial Ca9-22 cell death

Cited by 3 publications

References 24 publications

Reactive oxygen species generation required for autophagy induction during butyrate- or propionate-induced release of damage-associated molecular patterns from dying gingival epithelial Ca9-22 cells

Reactive oxygen species generation required for autophagy induction during butyrate- or propionate-induced release of damage-associated molecular patterns from dying gingival epithelial Ca9-22 cells

P38α contributes to TNF‐α‐induced IL‐8 production in human gingival cells

Role of the nucleotide-binding oligomerization domain-containing protein 1 pathway in the development of periodontitis

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