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Downregulation of the Long Non-Coding RNA Meg3 Promotes Angiogenesis After Ischemic Brain Injury by Activating Notch Signaling

Angiogenesis after ischemic brain injury contributes to the restoration of blood supply in the ischemic zone. Strategies to improve angiogenesis may facilitate the function recovery after stroke. Recent researches have demonstrated that dysfunction of long non-coding RNAs are associated with angioge...

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Autores principales: Liu, Juan, Li, Qing, Zhang, Kun-shan, Hu, Bin, Niu, Xin, Zhou, Shu-min, Li, Si-guang, Luo, Yu-ping, Wang, Yang, Deng, Zhi-feng
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer US 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5684256/
https://www.ncbi.nlm.nih.gov/pubmed/27900677
http://dx.doi.org/10.1007/s12035-016-0270-z
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author Liu, Juan
Li, Qing
Zhang, Kun-shan
Hu, Bin
Niu, Xin
Zhou, Shu-min
Li, Si-guang
Luo, Yu-ping
Wang, Yang
Deng, Zhi-feng
author_facet Liu, Juan
Li, Qing
Zhang, Kun-shan
Hu, Bin
Niu, Xin
Zhou, Shu-min
Li, Si-guang
Luo, Yu-ping
Wang, Yang
Deng, Zhi-feng
author_sort Liu, Juan
collection PubMed
description Angiogenesis after ischemic brain injury contributes to the restoration of blood supply in the ischemic zone. Strategies to improve angiogenesis may facilitate the function recovery after stroke. Recent researches have demonstrated that dysfunction of long non-coding RNAs are associated with angiogenesis. We have previously reported that long non-coding RNAs (lncRNAs) are aberrantly expressed in ischemic stroke. However, little is known about long non-coding RNAs and theirs role in angiogenesis after stroke. In this study, we identified a rat lncRNAs, Meg3, and found that Meg3 was significantly decreased after ischemic stroke. Overexpression of Meg3 suppressed functional recovery and decreased capillary density after ischemic stroke. Downregulation of Meg3 ameliorated brain lesion and increased angiogenesis after ischemic stroke. Silencing of Meg3 resulted in a proangiogenic effect evidenced by increased endothelial cell migration, proliferation, sprouting, and tube formation. Mechanistically, we showed that Meg3 negatively regulated notch pathway both in vivo and in vitro. Inhibition of notch signaling in endothelial cells reversed the proangiogenic effect induced by Meg3 downregulation. This study revealed the function of Meg3 in ischemic stroke and elucidated its mechanism in angiogenesis after ischemic stroke. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1007/s12035-016-0270-z) contains supplementary material, which is available to authorized users.
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spelling pubmed-56842562017-11-27 Downregulation of the Long Non-Coding RNA Meg3 Promotes Angiogenesis After Ischemic Brain Injury by Activating Notch Signaling Liu, Juan Li, Qing Zhang, Kun-shan Hu, Bin Niu, Xin Zhou, Shu-min Li, Si-guang Luo, Yu-ping Wang, Yang Deng, Zhi-feng Mol Neurobiol Article Angiogenesis after ischemic brain injury contributes to the restoration of blood supply in the ischemic zone. Strategies to improve angiogenesis may facilitate the function recovery after stroke. Recent researches have demonstrated that dysfunction of long non-coding RNAs are associated with angiogenesis. We have previously reported that long non-coding RNAs (lncRNAs) are aberrantly expressed in ischemic stroke. However, little is known about long non-coding RNAs and theirs role in angiogenesis after stroke. In this study, we identified a rat lncRNAs, Meg3, and found that Meg3 was significantly decreased after ischemic stroke. Overexpression of Meg3 suppressed functional recovery and decreased capillary density after ischemic stroke. Downregulation of Meg3 ameliorated brain lesion and increased angiogenesis after ischemic stroke. Silencing of Meg3 resulted in a proangiogenic effect evidenced by increased endothelial cell migration, proliferation, sprouting, and tube formation. Mechanistically, we showed that Meg3 negatively regulated notch pathway both in vivo and in vitro. Inhibition of notch signaling in endothelial cells reversed the proangiogenic effect induced by Meg3 downregulation. This study revealed the function of Meg3 in ischemic stroke and elucidated its mechanism in angiogenesis after ischemic stroke. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1007/s12035-016-0270-z) contains supplementary material, which is available to authorized users. Springer US 2016-11-29 2017 /pmc/articles/PMC5684256/ /pubmed/27900677 http://dx.doi.org/10.1007/s12035-016-0270-z Text en © The Author(s) 2016 Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided 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.
spellingShingle Article
Liu, Juan
Li, Qing
Zhang, Kun-shan
Hu, Bin
Niu, Xin
Zhou, Shu-min
Li, Si-guang
Luo, Yu-ping
Wang, Yang
Deng, Zhi-feng
Downregulation of the Long Non-Coding RNA Meg3 Promotes Angiogenesis After Ischemic Brain Injury by Activating Notch Signaling
title Downregulation of the Long Non-Coding RNA Meg3 Promotes Angiogenesis After Ischemic Brain Injury by Activating Notch Signaling
title_full Downregulation of the Long Non-Coding RNA Meg3 Promotes Angiogenesis After Ischemic Brain Injury by Activating Notch Signaling
title_fullStr Downregulation of the Long Non-Coding RNA Meg3 Promotes Angiogenesis After Ischemic Brain Injury by Activating Notch Signaling
title_full_unstemmed Downregulation of the Long Non-Coding RNA Meg3 Promotes Angiogenesis After Ischemic Brain Injury by Activating Notch Signaling
title_short Downregulation of the Long Non-Coding RNA Meg3 Promotes Angiogenesis After Ischemic Brain Injury by Activating Notch Signaling
title_sort downregulation of the long non-coding rna meg3 promotes angiogenesis after ischemic brain injury by activating notch signaling
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5684256/
https://www.ncbi.nlm.nih.gov/pubmed/27900677
http://dx.doi.org/10.1007/s12035-016-0270-z
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