Page 73 - Read Online
P. 73

Qu et al. Neuroimmunol Neuroinflammation 2018;5:10            Neuroimmunology and
               DOI: 10.20517/2347-8659.2018.01                                   Neuroinflammation




               Review                                                                        Open Access


               MicroRNA-126 is a prospective target for vascular
               disease

               Mei-Jie Qu , Jia-Ji Pan , Xiao-Jing Shi , Zhi-Jun Zhang , Yao-Hui Tang , Guo-Yuan Yang 1,2
                                                               2
                                                 2
                                                                            2
                        1,2
                                   2
               1 Department of Neurology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.
               2 Neuroscience and Neuroengineering Research Centre, Med-X Research Institute and School of Biomedical Engineering, Shanghai Jiao
               Tong University, Shanghai 200030, China.
               Correspondence to: Dr. Guo-Yuan Yang, Neuroscience and Neuroengineering Research Center, Med-X Research Institute and School
               of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai 200030, China. E-mail: gyyang@sjtu.edu.cn
               How to cite this article: Qu MJ, Pan JJ, Shi XJ, Zhang ZJ, Tang YH, Yang GY. MicroRNA-126 is a prospective target for vascular
               disease. Neuroimmunol Neuroinflammation 2018;5:10. http://dx.doi.org/10.20517/2347-8659.2018.01

               Received: 3 Jan 2018     Frist Decision: 26 Feb 2018    Revised: 26 Mar 2018    Accepted: 26 Mar 2018      Published: 9 Apr 2018
               Science Editor: Athanassios P. Kyritsis    Copy Editor: Jun-Yao Li    Production Editor: Huan-Liang Wu



               Abstract
               MicroRNA-126 was involved in angiogenesis during physiological and pathological process. It was mainly expressed in
               endothelial cells, and defined as a pivotal biological molecule associated with vascular disease. Increased microRNA-126
               in endothelial cells promotes angiogenesis in ischemic stroke, repairs impaired endothelial cells in atherosclerosis, and
               attenuates vascular dysfunction in diabetics. By contrast, microRNA-126 transferred from endothelial cell to smooth
               muscle cells could lead to proliferation that induced intimal hyperplasia. Additionally, microRNA-126 could be a tumor
               suppressor or an oncogene, which was depended on the cancer type. In this review, we summarized the function of
               microRNA-126 in ischemic stroke, atherosclerosis, diabetics, tumor, and discussed the underlying mechanisms.

               Keywords: Atherosclerosis, diabetes, ischemia, microRNA-126





               INTRODUCTION
               MicroRNAs (miRNAs) are 20-22 nucleotides single-strand and non-coding RNA, which are involved in
               regulating diverse cellular processes. MiRNAs are originally transcribed from portion of introns of mRNA
                                          [1]
               or independent miRNA genes . MiRNAs regulate gene expression through Ago2-RISC or Ago1-RISC,
                                                                            [2]
               which depends on if miRNA precisely matched with its target sequence .
               MicroRNA-126 (miR-126) is located in an intron of the epidermal growth factor-like-domain 7 gene
               (EGFL7). The pri-miR-126 is transcribed from EGFL7 by RNA polymerase II. With the aid of RNase III


                           © The Author(s) 2018. Open Access This article is licensed under a Creative Commons Attribution 4.0
                           International License (https://creativecommons.org/licenses/by/4.0/), which permits unrestricted use,
                sharing, adaptation, distribution and reproduction in any medium or format, for any purpose, even commercially, as long
                as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license,
                and indicate if changes were made.


                                                                                                                                                      www.nnjournal.net
   68   69   70   71   72   73   74   75   76   77   78