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超homocysteine通过mTOR介导的自和连接素表达抑制促进白内障的发展
Wen-Na Liu1, Hong-Lang Huang2, Yu Lan1
1Department of Laboratory Medicine and Sichuan Provincial Key Laboratory for Human Disease Gene Study, Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, China.
International immunopharmacology
|August 8, 2024
概括
高水平的同类氨酸 (Hcy) 与白内障有关. 这项研究表明,Hcy通过mTOR途径扰乱了自和连xin表达,可能导致白内障的发展.
科学领域:
- 眼科医生 眼科 眼科
- 细胞生物学 细胞生物学
- 生物化学 生物化学
背景情况:
- 超homocysteinemia是各种疾病的独立风险因素,包括眼部疾病.
- 高水平的同类氨酸 (Hcy) 已与眼睛疾病有关,但白内障形成的具体机制需要阐明.
研究的目的:
- 调查高水平的同类素 (Hcy) 与白内障发展之间的关联.
- 探索在Hcy诱导白内障中mTOR介导的自和连xin表达的作用.
主要方法:
- 在白内障患者和对照者中,使用液态染色体协同质谱测量血清Hcy水平.
- 人类透镜上皮细胞 (HLC-B3) 用Hcy进行治疗,以分析自标记物,连xin表达和细胞内.
- 西部涂抹评估了酸化mTOR (p-mTOR) 和自标志物;光显微镜观察到自真空孔和Ca2+.
- 救援实验使用了mTOR抑制剂拉巴素来逆转HCY诱导的影响.
主要成果:
- 白内障患者的血清Hcy水平明显高于健康对照组.
- 在HLC-B3细胞中,HCY治疗抑制了自标志物 (LC3B,Beclin1) 和连接素 (Cx43,Cx50).
- Hcy诱导了细胞内Ca2+积累,与减少连素表达有关,并增加了p-mTOR.
- 拉帕米辛治疗挽救了自和连xin 的表达,减轻了 Hcy 的影响.
结论:
- 超homocysteinemia可能通过通过mTOR通路调节失调自,促进白内障的发展.
- 减少连素表达和随后的细胞内积累与Hcy诱导的白内障有关.
- 针对mTOR途径为与Hcy相关的白内障提供了潜在的治疗策略.
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