中国神经再生研究(英文版) ›› 2021, Vol. 16 ›› Issue (9): 1877-1881.doi: 10.4103/1673-5374.306098

• 原著:视神经损伤修复保护与再生 • 上一篇    下一篇

长链非编码RNA心肌梗死相关转录本对早产儿视网膜病变中视网膜新血管形成的影响

  

  • 出版日期:2021-09-15 发布日期:2021-02-05
  • 基金资助:

    国家自然科学基金项目(81600747);辽宁省医学创业基金(201501020

Effects of long non-coding RNA myocardial infarction-associated transcript on retinal neovascularization in a newborn mouse model of oxygen-induced retinopathy

Yu Di, Yue Wang, Xue Wang, Qing-Zhu Nie*   

  1. Department of Ophthalmology, Shengjing Hospital of China Medical University, Shenyang, Liaoning Province, China
  • Online:2021-09-15 Published:2021-02-05
  • Contact: Qing-Zhu Nie, PhD, 390532915@qq.com
  • Supported by:
    This study was supported by the National Natural Science Foundation of China, No. 81600747 (to YD) and the Start-Up Foundation for Doctors of Liaoning Province, China, No. 201501020 (to YD).

摘要:

长链非编码RNA-心肌梗死相关转录本是否可能参与早产儿视网膜病变?实验设计希望验证这一假设,(1)构建了模拟早产儿视网膜病变模型:给予8d龄新生小鼠以75±2%氧气干预至12d龄后恢复常氧,建立氧诱导性视网膜病变模型;(2)干预:小鼠出生后第11天通过玻璃体注射心肌梗死相关转录本siRNA质粒以敲减长链非编码RNA-心肌梗死相关转录本;(3)结果发现:心肌梗死相关转录本siRNA转染后可显著抑制心肌梗死相关转录本mRNA的表达,使模型小鼠视网膜病理损伤明显减轻,同时降低视网膜中磷酸化磷脂酰肌醇 3-激酶、磷酸化AKT和血管内皮生长因子的免疫阳性反应、蛋白和基因表达;(4)结果证实:心肌梗死相关转录本可参与了早产儿视网膜病变中发生的新生血管形成,且抑制心肌梗死相关转录本可下调磷脂酰肌醇 3-激酶、AKT和血管内皮生长因子的表达,产生抑制新生血管形成的效应。实验于2016年2月25日经中国医科大学附属盛京医院院伦理委员会批准,批准号2016PS074K。

https://orcid.org/0000-0003-4749-2084 (Qing-Zhu Nie)

关键词:

视网膜病变, 长链非编码RNA, 心肌梗死相关转录本, 血管内皮生长因子, 早产, 新血管形成, 神经血管, 血管发育

Abstract: Whether long non-coding RNA myocardial infarction-associated transcript is involved in oxygen-induced retinopathy remains poorly understood. To validate this hypothesis, we established a newborn mouse model of oxygen-induced retinopathy by feeding in an oxygen concentration of 75 ± 2% from postnatal day 8 to postnatal day 12, followed by in normal air. On postnatal day 11, the mice were injected with the myocardial infarction-associated transcript siRNA plasmid via the vitreous cavity to knockdown long non-coding RNA myocardial infarction-associated transcript. Myocardial infarction-associated transcript siRNA transcription significantly inhibited myocardial infarction-associated transcript mRNA expression, reduced the phosphatidylinosital-3-kinase, phosphorylated Akt and vascular endothelial growth factor immunopositivities, protein and mRNA expression, and alleviated the pathological damage to the retina of oxygen-induced retinopathy mouse models. These findings suggest that myocardial infarction-associated transcript is likely involved in the retinal neovascularization in retinopathy of prematurity and that inhibition of myocardial infarction-associated transcript can downregulate phosphatidylinosital-3-kinase, phosphorylated Akt and vascular endothelial growth factor expression levels and inhibit neovascularization. This study was approved by the Animal Ethics Committee of Shengjing Hospital of China Medical University, China (approval No. 2016PS074K) on February 25, 2016. 

Key words: long non-coding RNA, myocardial infarction-associated transcript, neovascularization, neurovascular, prematurity, retinopathy, vascular development, vascular endothelial growth factor