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.

IF 1.9 4区 医学 Q2 DENTISTRY, ORAL SURGERY & MEDICINE
Journal of oral science Pub Date : 2024-04-16 Epub Date: 2024-03-15 DOI:10.2334/josnusd.23-0421
Kiwa Miyake, Yoshikazu Mikami, Takayuki Asayama, Taku Toriumi, Keiji Shinozuka, Morio Tonogi, Yoshiyuki Yonehara, Hiromasa Tsuda
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引用次数: 0

Abstract

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.

丁酸盐或丙酸盐诱导濒死牙龈上皮 Ca9-22 细胞释放损伤相关分子模式时,自噬诱导过程中需要产生活性氧。
目的:成熟牙菌斑中的细菌细胞会产生高浓度的短链脂肪酸(SCFA),如丁酸盐和丙酸盐。对人类牙龈上皮 Ca9-22 细胞进行 SCFA 处理可诱导细胞死亡。然而,细胞死亡的确切机制仍不清楚。方法:用丁酸盐或丙酸盐处理人牙龈上皮 Ca9-22 细胞以诱导细胞死亡,并用 SYTOX 绿色染料测量死亡细胞的数量。ATG5的siRNA和N-乙酰半胱氨酸(NAC)分别用于减少自噬和清除ROS。用Western印迹法检测损伤相关分子模式(DAMPs)的释放,如Sin3A相关蛋白130(SAP130)和高迁移率基团框1(HMGB1):结果:减少自噬可明显抑制 SCFA 诱导的 Ca9-22 细胞死亡。SCFA处理后会产生ROS,用NAC清除ROS可减少细胞死亡。NAC 还减少了 SCFA 诱导的微管相关蛋白 1 轻链 3B (LC3B)-I 和 LC3B-II 的增加,并减轻了 DAMPs 的释放:结论:研究结果表明,ROS 的产生是自噬的必要条件,而自噬是 SCFA 诱导的细胞死亡和伴随的 DAMP 释放所必需的。
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来源期刊
Journal of oral science
Journal of oral science DENTISTRY, ORAL SURGERY & MEDICINE-MATERIALS SCIENCE, BIOMATERIALS
CiteScore
3.80
自引率
0.00%
发文量
58
期刊介绍: Information not localized
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