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Lnc-216调节miR-143-5p / MMP2信号轴加剧视网膜内皮细胞功能障碍

Fang Wang¹, Zhangmei Guo¹, Guiqi Yang¹

¹Department of Ophthalmology, The Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan, China.

Clinical hemorheology and microcirculation

|June 29, 2024

概括

长非编码RNA LOC681216 (LNC-216) 通过海绵化miR-143-5p加剧糖尿病视网膜病变 (DR),增加MMP2表达并损害视网膜血管功能. 对于DR来说,LNC-216是一个潜在的治疗点.

科学领域:

眼科医生眼科眼科
分子生物学分子生物学
血管生物学血管生物学

背景情况:

糖尿病视网膜病变 (DR) 是糖尿病的一种严重并发症,导致视力丧失.
视网膜血管功能障碍是DR的关键病理特征.
长非编码RNAs (lncRNAs) 在DR病变发生中的作用是一个新兴的研究领域.

研究的目的:

调查LOC681216 (LNC-216) 在糖尿病视网膜血管功能障碍中的参与.
阐明LNC-216在高葡萄糖诱导的视网膜内皮细胞功能障碍中的作用背后的分子机制.

主要方法:

使用的老鼠视网膜微血管内皮细胞 (RRMECs) 暴露于高葡萄糖 (HG).
使用Clariom D Affymetrix平台进行基因表达分析.
通过伤口愈合,Transwell和血管管形成试验评估细胞迁移,入侵和管形成.
使用双露西法酶记者测定证实了相互作用.

主要成果:

在高温条件下的RRMEC中,LNC-216表达得到了上调.
击败LNC-216显著抑制了RRMEC迁移,伤口愈合和管道形成.
LNC-216作为miR-143-5p的分子海绵,导致矩阵金属酶2 (MMP2) 表达的增加.

结论:

通过miR-143-5p/MMP2通路,LNC-216会加剧糖尿病视网膜血管功能障碍.
针对LNC-216/miR-143-5p/MMP2轴为糖尿病视网膜病变提供了一个潜在的治疗策略.

关键词:

在Lnc-21616中,我们可以看到这就是MMP2的MMP2.糖尿病视网膜病变糖尿病视网膜病变在 miR-143-5p 中使用.微阵列是微阵列中的一个.

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