Long non-coding RNA-MIAT promotes neurovascular remodeling in the eye and brain.
Long non-coding RNA-MIAT promotes neurovascular remodeling in the eye and brain.
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长非编码RNA-MIAT促进眼睛和大脑的神经血管重塑
DOI：
10.18632/oncotarget.10434
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发表时间：
2016-08-02
期刊：
影响因子：
--
通讯作者：
Yan B
中科院分区：
文献类型：
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作者：
Jiang Q;Shan K;Qun-Wang X;Zhou RM;Yang H;Liu C;Li YJ;Yao J;Li XM;Shen Y;Cheng H;Yuan J;Zhang YY;Yan B
虽然神经和血管系统在功能上不同，但它们通常具有相似的功能维持机制。神经血管功能障碍已成为几种血管和神经疾病的发病机制。在这里，我们表明，长的非编码RNA-MIAT异常表达的神经血管功能障碍的条件下。MIAT显示为血管功能障碍的调节剂，包括视网膜血管生成、角膜血管生成和血管通透性。MIAT还显示为糖尿病条件下视网膜神经变性的调节剂。在机制上，MIAT通过MIAT/miR-150- 5 p/VEGF网络调节神经和血管细胞功能。眼是研究中枢神经系统（CNS）疾病的有价值的模型。我们发现，MIAT敲低导致脑微血管变性，进行性神经元丢失和神经变性，和行为缺陷的中枢神经系统神经血管疾病，阿尔茨海默氏病。MIAT可能是治疗神经血管相关疾病的药理学靶点。
Although nervous and vascular systems are functionally different, they usually share similar mechanisms for function maintenance. Neurovascular dysfunction has became the pathogenesis of several vascular and nervous disorders. Here we show that long non-coding RNA-MIAT is aberrantly expressed under neurovascular dysfunction condition. MIAT is shown as a regulator of vascular dysfunction, including retinal angiogenesis, corneal angiogenesis, and vascular permeability. MIAT is also shown as a regulator of retinal neurodegeneration under diabetic condition. Mechanistically, MIAT regulates neural and vascular cell function via MIAT/miR-150-5p/VEGF network. The eye is a valuable model to study central nervous system (CNS) disorders. We show that MIAT knockdown leads to cerebral microvascular degeneration, progressive neuronal loss and neurodegeneration, and behavioral deficits in a CNS neurovascular disorder, Alzheimer's disease. MIAT may represent a pharmacological target for treating neurovascular-related disorders.