在急性眼睛高血压下,氨酸8缺乏会加剧视网膜质细胞损伤
Chengshou Zhang1, Naiji Yu1, Qiyu Qin1
1Eye Center, The Second Affiliated Hospital, School of Medicine, Zhejiang University, Zhejiang Provincial Key Laboratory of Ophthalmology, Zhejiang Provincial Clinical Research Center for Eye Diseases, Zhejiang Provincial Engineering Institute on Eye Diseases, Hangzhou, Zhejiang, China.
Investigative ophthalmology & visual science
|September 1, 2023
概括
氨酸8/18 (KRT8/18) 存在于视网膜质细胞 (RGCs) 中. 在急性眼高血压 (AOH) 鼠标模型中,KRT8 缺乏会使RGC损伤和亡恶化.
科学领域:
- 眼科医生 眼科 眼科
- 神经科学是一个神经科学.
- 细胞生物学 细胞生物学
背景情况:
- 氨酸8/18 (KRT8/18) 是细胞功能至关重要的中间丝蛋白.
- 它们在视网膜质细胞 (RGC) 和神经保护中的作用在很大程度上仍未被探索.
研究的目的:
- 研究KRT8/18在RGC中的存在和功能.
- 确定KRT8/18在急性眼高血压 (AOH) 的小鼠模型中的作用.
主要方法:
- 在人类和小鼠视网膜和初级RGC中分析了KRT8/18表达.
- 在小鼠中诱导了AOH,KRT8在RGC中被选择性地使用腺相关病毒 (AAV) 击倒.
- 评估了组织学变化,RGC损失,亡标记物和MAPK通路激活.
主要成果:
- 在所有视网膜层中发现了KRT8/18,在RGC中表达高,AOH后水平增加.
- 单靠KRT8的击落并没有造成RGC的损伤.
- 在AOH小鼠中,KRT8缺乏加剧了视网膜稀释,RGC亡和质激活,与MAPK通路失调有关.
结论:
- 通过异常的MAPK通路激活,KRT8缺乏会促进RGC亡和AOH中的神经退行.
- 针对KRT8是一个潜在的治疗策略,用于眼光神经病变.
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