LPS诱导SGPP2参与内皮细胞中的代谢重编程
Xin Yi1, Meng-Ling Chang1, Zeng-Ding Zhou1
1Department of Burn, Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Free radical biology & medicine
|September 13, 2023
概括
脂聚糖 (LPS) 改变了内皮细胞的新陈代谢,增强了糖解,增加了活性氧物种 (ROS). 氨酸-1-酸酶2 (SGPP2) 的上调改善了细胞功能,并抑制了HIF-1α的降解,为败血症引起的器官损伤提供了治疗点.
科学领域:
- 分子生物学分子生物学
- 细胞生物学 细胞生物学
- 生物化学 生物化学
背景情况:
- 败血症引起的器官功能障碍涉及增加的血管透性.
- 在脂多糖 (LPS) 刺激后,内皮细胞的代谢变化尚不清楚.
- 在早期炎症期间调查内皮细胞的代谢变化至关重要.
研究的目的:
- 研究LPS对人类静脉内皮细胞 (HUVECs) 的代谢作用.
- 阐明LPS诱导的代谢变化如何影响内皮细胞功能.
- 为了确定LPS诱导的内皮损伤的潜在治疗点.
主要方法:
- 在LPS刺激的HUVEC中分析mRNA表达,染色质开放度和代谢流量.
- 评估中心代谢的变化,包括糖解和线粒体功能.
- 研究脂代谢和氨酸-1-酸酶2 (SGPP2) 的作用.
主要成果:
- 拉皮质细胞刺激增强了糖解,减少了线粒体膜潜力,增加了反应性氧物种 (ROS) 生产.
- 脂代谢在转录组水平上发生了改变,在LPS刺激细胞和斑马鱼中观察到SGPP2上调.
- SGPP2过度表达改善了内皮细胞屏障功能和线粒体呼吸,但导致氧化呼吸链脱并抑制了HIF-1α降解.
结论:
- LPS显著改变内皮细胞的新陈代谢,影响关键的细胞功能.
- SGPP2在调节内皮细胞对LPS的反应中起着至关重要的作用.
- 鉴定的分子和生化过程为LPS诱导的内皮损伤和潜在的炎症性疾病治疗策略提供了洞察力.
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