Long non-coding RNA-MIAT promotes neurovascular remodeling in the eye and brain
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Qin Jiang1,*, Kun Shan1,2,*, Xiao Qun-Wang1,*, Rong-Mei Zhou1, Hong Yang1, Chang Liu1,2, Yu-Jie Li1, Jin Yao1, Xiu-Miao Li1, Yi Shen1, Hong Cheng3, Jun Yuan4, Yang-Yang Zhang5, Biao Yan2
1Eye Hospital, Nanjing Medical University, Nanjing, China
2Research Center, Eye & ENT Hospital, Shanghai Medical College, Fudan University, Shanghai, China
3Department of Neurology, Jiangsu Province Hospital, Nanjing, China
4Department of Neurology, Jiangsu Chinese Medicine Hospital, Nanjing, China
5Department of Cardiac Surgery, The First School of Clinical Medicine, Nanjing Medical University, Nanjing, China
*These authors contributed equally to this work
Biao Yan, email: email@example.com
Keywords: long non-coding RNA, angiogenesis, neurodegeneration, reactive glia
Received: October 07, 2015 Accepted: June 06, 2016 Published: July 06, 2016
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.
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