通过向miR-126-5p调节多发性糖尿病视网膜病变的MALAT1机制
Wei Zhao1,2,3,4,5, Yanli Liu1,2, Cairui Li3,4,5
1The Third Affiliated Hospital, Southern Medical University Guangzhou 510630, Guangdong, China.
American journal of translational research
|June 12, 2023
概括
糖尿病视网膜病变 (DR) 的进展涉及 lncRNA MALAT1 通过抑制 miR-126-5p 来促进病理血管生成. 针对这一轴可能为增殖性糖尿病视网膜病变 (PDR) 提供新的治疗策略.
科学领域:
- 眼科医生 眼科 眼科
- 分子生物学分子生物学
- 遗传学 是一个遗传学.
背景情况:
- 糖尿病视网膜病变 (DR) 是导致失明的首要原因,通常会发展为多发性糖尿病视网膜病变 (PDR),其特征是视网膜新血管化.
- 了解驱动PDR病变的分子机制对于开发有效的治疗方法至关重要.
研究的目的:
- 调查长非编码RNAMALAT1 (MALAT1) 及其与miR-126-5p相互作用在增殖性糖尿病视网膜病变 (PDR) 的进展中的作用.
主要方法:
- 使用暴露于高葡萄糖的老鼠视网膜内皮细胞 (RECs) 建立了体外PDR模型.
- 使用siRNA降低了MALAT1的调节,使用miRNA模拟物提高了miR-126-5p的调节.
- 技术包括双露西法酶记者试验,RNA免疫沉,管状形成试验,CCK-8试验,划痕试验,西斑和qPCR来评估分子相互作用和细胞功能.
主要成果:
- 在REC中,高葡萄糖诱导了MALAT1上调和miR-126-5p下调.
- 降低MALAT1或提高miR-126-5p的调节抑制了高葡萄糖诱导的RECs的血管生成,增殖和迁移.
- 减少了VEGF,MMP-2和MMP-9水平,并证实MALAT1直接向和抑制miR-126-5p.
结论:
- 马拉特1/miR-126-5p轴在PDR病变发生过程中起着重要作用.
- 通过抑制miR-126-5p,MALAT1促进PDR,从而诱导REC的增殖,迁移和血管生成.
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