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

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          Abstract

          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.

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          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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          lncRNA-MIAT regulates microvascular dysfunction by functioning as a competing endogenous RNA.

          Biao Yan, Jin-Feng Yao, Jing-Yu Liu … (2015)
          Pathological angiogenesis is a critical component of diseases, such as ocular disorders, cancers, and atherosclerosis. It is usually caused by the abnormal activity of biological processes, such as cell proliferation, cell motility, immune, or inflammation response. Long noncoding RNAs (lncRNAs) have emerged as critical regulators of these biological processes. However, the role of lncRNA in diabetes mellitus-induced microvascular dysfunction is largely unknown.
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            A pituitary-derived MEG3 isoform functions as a growth suppressor in tumor cells.

            Xun Zhang, Staci Scolavino, Daniel Danila … (2003)
            Human pituitary adenomas are the most common intracranial neoplasm. Typically monoclonal in origin, a somatic mutation is a prerequisite event in tumor development. To identify underlying pathogenetic mechanisms in tumor formation, we compared the difference in gene expression between normal human pituitary tissue and clinically nonfunctioning pituitary adenomas by cDNA-representational difference analysis. We cloned a cDNA, the expression of which was absent in these tumors, that represents a novel transcript from the previously described MEG3, a maternal imprinting gene with unknown function. It was expressed in normal human gonadotrophs, from which clinically nonfunctioning pituitary adenomas are derived. Additional investigation by Northern blot and RT-PCR demonstrated that this gene was also not expressed in functioning pituitary tumors as well as many human cancer cell lines. Moreover, ectopic expression of this gene inhibits growth in human cancer cells including HeLa, MCF-7, and H4. Genomic analysis revealed that MEG3 is located on chromosome 14q32.3, a site that has been predicted to contain a tumor suppressor gene involved in the pathogenesis of meningiomas. Taken together, our data suggest that MEG3 may represent a novel growth suppressor, which may play an important role in the development of human pituitary adenomas.
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              Role of angiogenesis in patients with cerebral ischemic stroke.

              Parvathi Kumar, Jian Wang, N. A. P. Kiran Kumar … (1994)
              Stroke is one of the most common causes of mortality and morbidity in the Western world. It results from the occlusion of a cerebral artery followed by severe disturbances in blood supply through microvessels to brain tissue. Despite an extensive literature its pathophysiology is poorly understood, and this has severely impeded the logical development of therapy. Brains were obtained from 10 patients aged 46 to 85 years with survival times of 5 to 92 days after their stroke. Infarcted areas and representative control tissues from the contralateral uninvolved brain hemisphere were collected. Microvessel density was measured microscopically. A total of 6520 microvessels were scored in 10,801 areas. The level of activation of the endothelial cells was studied by immunohistochemistry using three monoclonal antibodies, viz, E-9, raised against activated endothelial cells; IG11, recognizing vascular cell adhesion molecule-1; and anti-proliferating cell nuclear antigen. Angiogenic activity in tissue extracts was examined using an in vivo chicken chorioallantoic membrane assay. There was a statistically significant increase in the number of microvessels (Wilcoxon log-rank test; P < or = .01) in 9 of 10 infarcted brain tissues when compared with their contralateral normal hemisphere. In these patients the higher blood vessel counts correlated with longer survival, as ascertained by Spearman's p analysis (P < .02). The number of microvessels filled with blood cells was significantly lower in the infarcted hemispheres (P < .01). In contrast, statistically significant increased numbers of empty microvessels occurred in infarcted tissues compared with the contralateral hemisphere. Monoclonal antibody E-9 reacted weakly with normal-brain vascular endothelial cells; anti-proliferating cell nuclear antigen and IG11 were virtually negative. All three antibodies strongly stained the blood vessels of stroke tissues. The stroke tissues contained angiogenic activity, as shown by the induction of new blood vessels in a chorioallantoic membrane assay. We have shown that stroke causes active angiogenesis that is more developed in the penumbra. Further experiments are needed to determine if this angiogenesis has beneficial effect.
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                Author and article information

                Contributors
                Qing Li: 86-21-24056319 , liqing_236@aliyun.com
                Yang Wang: 86-21-24056319 , wangy63cn@126.com
                Zhi-feng Deng: 86-21-38297188 , dengzf63@126.com
                Journal
                Journal ID (nlm-ta): Mol Neurobiol
                Journal ID (iso-abbrev): Mol. Neurobiol
                Title: Molecular Neurobiology
                Publisher: Springer US (New York )
                ISSN (Print): 0893-7648
                ISSN (Electronic): 1559-1182
                Publication date (Electronic): 29 November 2016
                Publication date PMC-release: 29 November 2016
                Publication date (Print): 2017
                Volume: 54
                Issue: 10
                Pages: 8179-8190
                Affiliations
                [1 ]ISNI 0000 0004 1798 5117, GRID grid.412528.8, Department of Neurosurgery, , Shanghai Jiao Tong University Affiliated Sixth People’s Hospital, ; Shanghai, China
                [2 ]ISNI 0000 0004 1798 5117, GRID grid.412528.8, Institute of Microsurgery on Extremities, , Shanghai Jiao Tong University Affiliated Sixth People’s Hospital, ; Shanghai, China
                [3 ]ISNI 0000000123704535, GRID grid.24516.34, Stem Cell Translational Research Center, Tongji Hospital, , Tongji University School of Medicine, ; Shanghai, China
                Article
                Publisher ID: 270
                DOI: 10.1007/s12035-016-0270-z
                PMC ID: 5684256
                PubMed ID: 27900677
                SO-VID: 7133d0f2-1119-4df8-9479-738cee507cbc
                Copyright © © The Author(s) 2016
                License:

                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.

                History
                Date received : 28 July 2016
                Date accepted : 30 October 2016
                Funding
                Funded by: the National Natural Science Foundation of China
                Award ID: 81272170
                Award ID: 81471243
                Award Recipient :
                Categories
                Subject: Article
                Custom metadata
                issue-copyright-statement © Springer Science+Business Media, LLC 2017

                ScienceOpen disciplines: Neurosciences
                Keywords: lncrnas,meg3,ischemic stroke,angiogenesis,notch pathway
                Data availability:
                ScienceOpen disciplines: Neurosciences
                Keywords: lncrnas, meg3, ischemic stroke, angiogenesis, notch pathway

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