通过miR-19a-3p/PTEN调节抑制自,保护视网膜色素上皮细胞免受高血糖损伤
Qiaoyun Gong1, Dawei Luo1, Haiyan Wang1
1Department of Ophthalmology, Shanghai General Hospital, Shanghai Jiao Tong University, Shanghai, China; National Clinical Research Center for Eye Diseases, Shanghai, China; Shanghai Key Laboratory of Ocular Fundus Diseases, Shanghai, China; Shanghai Engineering Center for Visual Science and Photomedicine, Shanghai, China; Shanghai Engineering Center for Precise Diagnosis and Treatment of Eye Disease, Shanghai, China.
概括
糖尿病视网膜病变 (DR) 涉及异常的自. 上调微RNA (miR)-19a-3p通过向PTEN来抑制这一过程,保护视网膜细胞并为DR提供潜在的治疗方法.
科学领域:
- 眼科医生 眼科 眼科
- 细胞生物学 细胞生物学
- 分子生物学分子生物学
背景情况:
- 糖尿病视网膜病变 (DR) 是糖尿病的并发症,影响视网膜.
- 细胞降解过程自的作用在DR病原发生过程中尚未完全理解.
- 了解DR中自的分子机制对于开发有效治疗是至关重要的.
研究的目的:
- 研究自在糖尿病视网膜病变 (DR) 中的作用和分子机制.
- 探索微RNA (miR)-19a-3p作为DR治疗点的潜力.
主要方法:
- 在体内糖尿病大鼠和体内高血糖视网膜色素表皮质 (RPE) 细胞模型中建立.
- 使用传输电子显微镜和mRFP-GFP-LC3腺病毒分析了自流.
- 量化了miR-19a-3p,PTEN/Akt/mTOR通路组件,以及与自相关的蛋白质 (LC3II/I,p62).
- 通过各种测试评估了RPE细胞的亡,迁移,活力和透性.
主要成果:
- 在DR模型中,自细胞与自细胞积累一起异常激活了自细胞.
- DR诱导了PTEN表达,抑制了Akt/mTOR,并促进了自和亡.
- miR-19a-3p直接针对PTEN,扭转了这些DR相关的变化.
- 通过miR-19a-3p,PTEN淘汰或3MA治疗保护的RPE细胞降低自的调节.
结论:
- 通过针对PTEN,对miR-19a-3p的上调抑制异常自,保护RPE细胞免受DR损伤.
- miR-19a-3p显示出作为一种新的治疗点,可以在早期DR中诱导保护性自.
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