在高血糖条件下,骨髓干细胞中长非编码RNA DINO 和 ROR 的表达
Sanaz Tavakoli1, Hamidreza Vaziri1, Mahshid Hodjat2
1Department of Biology, Faculty of Science, University of Guilan, Rasht, Iran.
Journal of diabetes and metabolic disorders
|January 6, 2026
概括
高水平的葡萄糖会通过增加氧化应激和DNA损伤来损害介质干细胞 (MSC),从而影响它们的再生潜力. 长非编码RNAROR和DINO参与MSC对这种损伤的反应.
科学领域:
- 细胞生物学 细胞生物学
- 分子生物学分子生物学
- 干细胞生物学 干细胞生物学
背景情况:
- 糖尿病是一种代谢障碍,导致广泛的器官并发症.
- 介酶干细胞 (MSCs) 对于组织修复至关重要,但因高血糖 (高血糖) 而受损.
- 长非编码RNAs (lncRNAs) 影响细胞对压力和DNA损伤的反应.
研究的目的:
- 调查MSCs中高血糖引起的氧化损伤.
- 探索 lncRNA ROR 和 lncRNA DINO 在这个过程中的作用.
主要方法:
- 暴露骨髓衍生MSCs高葡萄糖 (30mM或40mM) 3或9天.
- 对氧化应激和对DNA损伤的彗星测试进行了评估.
- 通过qRT-PCR对P53,P21,IncRNA ROR和IncRNA DINO的基因表达量化.
主要成果:
- 高血糖症显著增加ROS水平和DNA损伤.
- 在高葡萄糖条件下,P53和P21的表达增加.
- lncRNA DINO是上调的,而 lncRNA ROR是下调的.
结论:
- 长期高血糖会导致MSC的氧化应激和DNA损伤,可能通过P53/P21通路.
- lncRNA ROR和lncRNA DINO在MSCs对葡萄糖诱导的压力的反应中起作用.
- 了解这些机制对于在糖尿病中保持MSC功能至关重要.
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