来自BMSCs的外体通过携带miR-483-5p缓解高葡萄糖诱导的糖尿病视网膜病变
Dan Cao1, Liang Zhou1, Rong Hu2
1Department of Ophthalmology, The Second Xiangya Hospital of Central South University, Changsha, Hunan Province, People's Republic of China.
Journal of biochemical and molecular toxicology
|December 9, 2023
概括
带有miR-483-5p的骨髓介质干细胞外体会抑制糖尿病视网膜病变 (DR) 的进展. 这一发现为DR提供了一个新的治疗策略,通过保护视网膜细胞免受高葡萄糖诱导的损伤.
科学领域:
- 眼科医生 眼科 眼科
- 细胞生物学 细胞生物学
- 生物技术是生物技术.
背景情况:
- 糖尿病视网膜病变 (DR) 是糖尿病的一个渐进的并发症.
- 骨髓介质干细胞 (BMSCs) 分泌的外体显示出调节DR的潜力.
- 在DR中的这些外体内,miR-483-5p的作用在很大程度上是未知的.
研究的目的:
- 调查携带miR-483-5p的BMSC衍生外体是否可以调节糖尿病视网膜病变 (DR) 的进展.
- 探索涉及胰岛素样生长因子1受体 (IGF-1R) 的潜在机制.
主要方法:
- 在实验室中,ARPE-19细胞被高葡萄糖 (HG) 处理,以模仿DR.
- 外体从BMSC中分离出来并进行了表征.
- 细胞活力,细胞亡,miR-483-5p和IGF-1R水平使用CCK-8,流式细胞计量,qRT-PCR和西白斑等测试进行了评估.
- 双化酶测定证实了miR-483-5p和IGF-1R之间的相互作用.
主要成果:
- 在ARPE-19细胞中,HG诱导了显著的亡.
- 由BMSCs衍生的外体保护ARPE-19细胞免受HG诱导的亡.
- 在外体体中抑制miR-483-5p加剧了细胞亡.
- 鉴定出IGF-1R是miR-483-5p的直接标,其沉默反转了对外体的保护作用,降低了miR-483-5p的调控.
结论:
- 由BMSCs衍生出来的外体通过输送miR-483-5p.p.来抑制DR的进展.
- miR-483-5p/IGF-1R轴是这些外体的保护作用的关键机制.
- 这项研究为针对糖尿病视网膜病变的新型治疗策略提供了理论基础.
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