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LncRNA-XIST Promotes Proliferation and Migration in ox-LDL Stimulated Vascular Smooth Muscle Cells through miR-539-5p/SPP1 Axis

Long noncoding RNAs (lncRNAs) are untranslated transcripts greater than 200 nucleotides in length. Despite not being translated, they play a role in the regulation of transcription, translation, and other cellular processes and have been identified as key regulator in the progression of atherosclero...

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Autores principales: Zhang, Yi, Tang, Yong, Yan, Jianhua
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8752241/
https://www.ncbi.nlm.nih.gov/pubmed/35028010
http://dx.doi.org/10.1155/2022/9911982
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author Zhang, Yi
Tang, Yong
Yan, Jianhua
author_facet Zhang, Yi
Tang, Yong
Yan, Jianhua
author_sort Zhang, Yi
collection PubMed
description Long noncoding RNAs (lncRNAs) are untranslated transcripts greater than 200 nucleotides in length. Despite not being translated, they play a role in the regulation of transcription, translation, and other cellular processes and have been identified as key regulator in the progression of atherosclerosis. This study focused on the lncRNA X-inactive specific transcript (XIST), which participates in the regulation of X chromosome inactivation. XIST is produced by the XIST gene and is located on human chromosome Xql3.2. We also focused on discovering the possible role and mechanism of lncRNA XIST in oxidized low-density lipoprotein- (ox-LDL-) stimulated vascular smooth muscle cells (VSMCs), which could further help evalute its possible a role in the progression of atherosclerosis. XIST was overexpressed in ox-LDL-stimulated VSMCs, while the expression of miR-539-5p was decreased. XIST knockdown hindered the proliferation and migration of ox-LDL-treated VSMCs. XIST inhibits the miR-539-5p expression through direct interaction. Besides, miR-539-5p inhibitors can partially reverse the effect of XIST depletion on the proliferation and migration of VSMCs induced by ox-LDL stimulation. Further mechanistic analysis showed that secreted phosphoprotein 1 (SPP1) is the target of miR-539-5p, and XIST acts as a competing endogenous RNA for miR-539-5p to enhance the expression of SPP1. In addition, miR-539-5p inhibitor exerts its proliferation and migration effects by activating the miR-539-5p/SPP1 axis in VSMCs stimulated by ox-LDL. In conclusion, our study findings show that XIST inhibition can inhibit the proliferation and migration of atherosclerosis vascular smooth muscle cells, which provides a new theoretical basis for atherosclerosis treatment.
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spelling pubmed-87522412022-01-12 LncRNA-XIST Promotes Proliferation and Migration in ox-LDL Stimulated Vascular Smooth Muscle Cells through miR-539-5p/SPP1 Axis Zhang, Yi Tang, Yong Yan, Jianhua Oxid Med Cell Longev Research Article Long noncoding RNAs (lncRNAs) are untranslated transcripts greater than 200 nucleotides in length. Despite not being translated, they play a role in the regulation of transcription, translation, and other cellular processes and have been identified as key regulator in the progression of atherosclerosis. This study focused on the lncRNA X-inactive specific transcript (XIST), which participates in the regulation of X chromosome inactivation. XIST is produced by the XIST gene and is located on human chromosome Xql3.2. We also focused on discovering the possible role and mechanism of lncRNA XIST in oxidized low-density lipoprotein- (ox-LDL-) stimulated vascular smooth muscle cells (VSMCs), which could further help evalute its possible a role in the progression of atherosclerosis. XIST was overexpressed in ox-LDL-stimulated VSMCs, while the expression of miR-539-5p was decreased. XIST knockdown hindered the proliferation and migration of ox-LDL-treated VSMCs. XIST inhibits the miR-539-5p expression through direct interaction. Besides, miR-539-5p inhibitors can partially reverse the effect of XIST depletion on the proliferation and migration of VSMCs induced by ox-LDL stimulation. Further mechanistic analysis showed that secreted phosphoprotein 1 (SPP1) is the target of miR-539-5p, and XIST acts as a competing endogenous RNA for miR-539-5p to enhance the expression of SPP1. In addition, miR-539-5p inhibitor exerts its proliferation and migration effects by activating the miR-539-5p/SPP1 axis in VSMCs stimulated by ox-LDL. In conclusion, our study findings show that XIST inhibition can inhibit the proliferation and migration of atherosclerosis vascular smooth muscle cells, which provides a new theoretical basis for atherosclerosis treatment. Hindawi 2022-01-04 /pmc/articles/PMC8752241/ /pubmed/35028010 http://dx.doi.org/10.1155/2022/9911982 Text en Copyright © 2022 Yi Zhang et al. https://creativecommons.org/licenses/by/4.0/This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Article
Zhang, Yi
Tang, Yong
Yan, Jianhua
LncRNA-XIST Promotes Proliferation and Migration in ox-LDL Stimulated Vascular Smooth Muscle Cells through miR-539-5p/SPP1 Axis
title LncRNA-XIST Promotes Proliferation and Migration in ox-LDL Stimulated Vascular Smooth Muscle Cells through miR-539-5p/SPP1 Axis
title_full LncRNA-XIST Promotes Proliferation and Migration in ox-LDL Stimulated Vascular Smooth Muscle Cells through miR-539-5p/SPP1 Axis
title_fullStr LncRNA-XIST Promotes Proliferation and Migration in ox-LDL Stimulated Vascular Smooth Muscle Cells through miR-539-5p/SPP1 Axis
title_full_unstemmed LncRNA-XIST Promotes Proliferation and Migration in ox-LDL Stimulated Vascular Smooth Muscle Cells through miR-539-5p/SPP1 Axis
title_short LncRNA-XIST Promotes Proliferation and Migration in ox-LDL Stimulated Vascular Smooth Muscle Cells through miR-539-5p/SPP1 Axis
title_sort lncrna-xist promotes proliferation and migration in ox-ldl stimulated vascular smooth muscle cells through mir-539-5p/spp1 axis
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8752241/
https://www.ncbi.nlm.nih.gov/pubmed/35028010
http://dx.doi.org/10.1155/2022/9911982
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