甲型玻丁毒素通过调节低氧/低氧化处理的内皮细胞中的内网压力来激活保护性自
Yinhua Zhao1, Huang Lin1, Jiaxing Ma1
1Plastic and Reconstructive Surgery, Beijing Anzhen Hospital, Capital Medical University, Chaoyang District, Beijing, 100029, China.
Heliyon
|July 24, 2023
概括
甲型玻尿素毒素 (BTXA) 通过诱导中度内质网膜 (ER) 应激和自,保护人类皮肤微血管内皮细胞免受缺血/再损伤. 这种细胞反应增强了细胞的生存和完整性,这表明了治疗点.
科学领域:
- 细胞生物学 细胞生物学
- 分子医学是分子医学.
- 伤口治愈研究研究 伤口治愈研究
背景情况:
- 毒素A型 (BTXA) 通过诱导自而显示出对皮肤片中缺血/反 (I/R) 损伤的保护作用.
- 在BTXA对人类皮肤微血管内皮细胞 (HDMECs) I / R损伤的保护机制中,内质网膜 (ER) 应激和自激活的作用仍然未被证明.
研究的目的:
- 调查ER应力自激活在BTXA介导的HDMECs对低氧和再氧化 (H/R) 损伤的保护中的作用.
- 确定最佳BTXA度的细胞保护及其对ER压力和自标志物的影响.
主要方法:
- 在H/R暴露之前,HDMECs被预处理了BTXA度的变化.
- 使用细胞计数套件8 (CCK8) 评估了细胞活力.
- 分析了ER压力 (GRP78,CHOP) 和自 (LC3II/I,Beclin-1) 标记者的蛋白质表达,通过西方斑点 (WB).
- 评估了ER压力调节剂 (Thapsigargin,4-phenylbutyrate) 和自抑制剂 (Bafilomycin A1) 的作用.
主要成果:
- H/R治疗显著增加了ER压力和自标志物.
- 最佳的BTXA预处理 (1.6 U/mL) 增强了细胞存活率和标记物表达.
- ER压力诱导剂/抑制剂和自抑制剂降低了BTXA的保护作用和调节的标记物表达.
- 由BTXA引起的中度ER压力会触发保护性自.
结论:
- BTXA预处理通过诱导中度ER压力来保护HDMECs免受H/R损伤,这反过来又激活了保护性自.
- 过度的ER压力及其完全抑制都会否定BTXA的细胞保护作用.
- 适度的ER压力和自对细胞寿命和功能完整性至关重要,呈现出潜在的治疗策略.
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