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Integrated analyses of lncRNAs microarray profiles and mRNA–lncRNA coexpression in smooth muscle cells under hypoxic and normoxic conditions

Hypoxia may cause abnormal proliferation and migration of the vascular smooth muscle cells (VSMCs) from the media to the intima. This contributes to vessel narrowing and accelerates the process of atherosclerosis. The association of the aberrant expression of long noncoding RNAs (lncRNAs) with the d...

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Autores principales: Zhao, Qinshuo, Sun, Dating, Li, Yuanyuan, Qin, Jin, Yan, JiangTao
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Portland Press Ltd. 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6443952/
https://www.ncbi.nlm.nih.gov/pubmed/30850398
http://dx.doi.org/10.1042/BSR20181783
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author Zhao, Qinshuo
Sun, Dating
Li, Yuanyuan
Qin, Jin
Yan, JiangTao
author_facet Zhao, Qinshuo
Sun, Dating
Li, Yuanyuan
Qin, Jin
Yan, JiangTao
author_sort Zhao, Qinshuo
collection PubMed
description Hypoxia may cause abnormal proliferation and migration of the vascular smooth muscle cells (VSMCs) from the media to the intima. This contributes to vessel narrowing and accelerates the process of atherosclerosis. The association of the aberrant expression of long noncoding RNAs (lncRNAs) with the development and progression of atherosclerosis is well known; however, it is not well investigated in hypoxic VSMCs. Using a microarray approach, we identified 1056 and 2804 differentially expressed lncRNAs and mRNAs, respectively, in hypoxic and normoxic mouse aorta smooth muscle (MOVAS) cells. Of them, we randomly chose several lncRNAs and validated the microarray data using the quantitative PCR (qPCR) assay. Advanced bioinformatics analyses indicated that the up-regulated mRNAs were mainly involved in inflammatory responses, lipid metabolism, clearance of amyloid-β peptide, citrate cycle (TCA cycle), TGF-β signaling, and chemokine signaling. The down-regulated mRNAs were mainly involved in the apoptosis pathway, glycerolipid metabolism, Wnt signaling pathway, and MAPK signaling pathway. The constructed coexpression network indicated interactions between 87 lncRNAs and ten mRNAs. In addition, we demonstrated that the silence of lncRNA NONMMUT002434 expression could abrogate the migration and proliferation of smooth muscle cells dramatically. Our data provide comprehensive evidence on the differential expression of lncRNAs and mRNAs in hypoxic MOVAS cells, which may be valuable biomarkers for atherosclerotic diseases, and thereby facilitating diagnosis of atherosclerosis.
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spelling pubmed-64439522019-04-16 Integrated analyses of lncRNAs microarray profiles and mRNA–lncRNA coexpression in smooth muscle cells under hypoxic and normoxic conditions Zhao, Qinshuo Sun, Dating Li, Yuanyuan Qin, Jin Yan, JiangTao Biosci Rep Research Articles Hypoxia may cause abnormal proliferation and migration of the vascular smooth muscle cells (VSMCs) from the media to the intima. This contributes to vessel narrowing and accelerates the process of atherosclerosis. The association of the aberrant expression of long noncoding RNAs (lncRNAs) with the development and progression of atherosclerosis is well known; however, it is not well investigated in hypoxic VSMCs. Using a microarray approach, we identified 1056 and 2804 differentially expressed lncRNAs and mRNAs, respectively, in hypoxic and normoxic mouse aorta smooth muscle (MOVAS) cells. Of them, we randomly chose several lncRNAs and validated the microarray data using the quantitative PCR (qPCR) assay. Advanced bioinformatics analyses indicated that the up-regulated mRNAs were mainly involved in inflammatory responses, lipid metabolism, clearance of amyloid-β peptide, citrate cycle (TCA cycle), TGF-β signaling, and chemokine signaling. The down-regulated mRNAs were mainly involved in the apoptosis pathway, glycerolipid metabolism, Wnt signaling pathway, and MAPK signaling pathway. The constructed coexpression network indicated interactions between 87 lncRNAs and ten mRNAs. In addition, we demonstrated that the silence of lncRNA NONMMUT002434 expression could abrogate the migration and proliferation of smooth muscle cells dramatically. Our data provide comprehensive evidence on the differential expression of lncRNAs and mRNAs in hypoxic MOVAS cells, which may be valuable biomarkers for atherosclerotic diseases, and thereby facilitating diagnosis of atherosclerosis. Portland Press Ltd. 2019-04-02 /pmc/articles/PMC6443952/ /pubmed/30850398 http://dx.doi.org/10.1042/BSR20181783 Text en © 2019 The Author(s). http://creativecommons.org/licenses/by/4.0/This is an open access article published by Portland Press Limited on behalf of the Biochemical Society and distributed under the Creative Commons Attribution License 4.0 (CC BY) (http://creativecommons.org/licenses/by/4.0/) .
spellingShingle Research Articles
Zhao, Qinshuo
Sun, Dating
Li, Yuanyuan
Qin, Jin
Yan, JiangTao
Integrated analyses of lncRNAs microarray profiles and mRNA–lncRNA coexpression in smooth muscle cells under hypoxic and normoxic conditions
title Integrated analyses of lncRNAs microarray profiles and mRNA–lncRNA coexpression in smooth muscle cells under hypoxic and normoxic conditions
title_full Integrated analyses of lncRNAs microarray profiles and mRNA–lncRNA coexpression in smooth muscle cells under hypoxic and normoxic conditions
title_fullStr Integrated analyses of lncRNAs microarray profiles and mRNA–lncRNA coexpression in smooth muscle cells under hypoxic and normoxic conditions
title_full_unstemmed Integrated analyses of lncRNAs microarray profiles and mRNA–lncRNA coexpression in smooth muscle cells under hypoxic and normoxic conditions
title_short Integrated analyses of lncRNAs microarray profiles and mRNA–lncRNA coexpression in smooth muscle cells under hypoxic and normoxic conditions
title_sort integrated analyses of lncrnas microarray profiles and mrna–lncrna coexpression in smooth muscle cells under hypoxic and normoxic conditions
topic Research Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6443952/
https://www.ncbi.nlm.nih.gov/pubmed/30850398
http://dx.doi.org/10.1042/BSR20181783
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