LncRNA XIST regulates atherosclerosis progression in ox-LDL-induced HUVECs

Long noncoding RNAs (lncRNAs) have been verified as vital regulators in human disease, including atherosclerosis. However, the precise role of X-inactive-specific transcript (XIST) in atherosclerosis remains unclear. The proliferation and apoptosis of human umbilical vein endothelial cells (HUVECs)...

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Autores principales:	Gao Hongmei, Guo Zhaohui
Formato:	article
Lenguaje:	EN
Publicado:	De Gruyter 2021
Materias:	xist mir-98-5p pappa ox-ldl huvecs Medicine R
Acceso en línea:	https://doaj.org/article/59efd9ddd39c46b5b28c3ea6ac1f0e90
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spelling	oai:doaj.org-article:59efd9ddd39c46b5b28c3ea6ac1f0e902021-12-05T14:10:53ZLncRNA XIST regulates atherosclerosis progression in ox-LDL-induced HUVECs2391-546310.1515/med-2021-0200https://doaj.org/article/59efd9ddd39c46b5b28c3ea6ac1f0e902021-01-01T00:00:00Zhttps://doi.org/10.1515/med-2021-0200https://doaj.org/toc/2391-5463Long noncoding RNAs (lncRNAs) have been verified as vital regulators in human disease, including atherosclerosis. However, the precise role of X-inactive-specific transcript (XIST) in atherosclerosis remains unclear. The proliferation and apoptosis of human umbilical vein endothelial cells (HUVECs) exposed to low-density lipoprotein (ox-LDL) were assessed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazol-3-ium bromide, and flow cytometry assays, correspondingly. The western blot assay was used to quantify protein expression. Lactate dehydrogenase activity and the concentrations of inflammatory factors were measured by matched kits. The real-time quantitative polymerase chain reaction (qPCR) was used to determine α-smooth muscle actin, smooth muscle protein 22-α, XIST, miR-98-5p, and pregnancy-associated plasma protein A (PAPPA) levels in HUVECs. The relationship among XIST, miR-98-5p, and PAPPA was analyzed by dual-luciferase reporter, RNA immunoprecipitation, and RNA pull-down assays. We found ox-LDL repressed proliferation and induced inflammation and apoptosis in HUVECs. Loss-of-functional experiment suggested that the downregulation of XIST overturned the ox-LDL-induced effects on HUVECs. Additionally, overexpression of miR-98-5p-induced effects on ox-LDL-stimulated HUVECs was abolished by upregulation of XIST. However, silencing of miR-98-5p strengthened the ox-LDL-induced effects on HUVECs by increasing expression of PAPPA. Mechanistically, XIST could regulate PAPPA expression in ox-LDL-induced HUVECs by sponging miR-98-5p, providing understanding for atherosclerosis.Gao HongmeiGuo ZhaohuiDe Gruyterarticlexistmir-98-5ppappaox-ldlhuvecsMedicineRENOpen Medicine, Vol 16, Iss 1, Pp 117-127 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	xist mir-98-5p pappa ox-ldl huvecs Medicine R
spellingShingle	xist mir-98-5p pappa ox-ldl huvecs Medicine R Gao Hongmei Guo Zhaohui LncRNA XIST regulates atherosclerosis progression in ox-LDL-induced HUVECs
description	Long noncoding RNAs (lncRNAs) have been verified as vital regulators in human disease, including atherosclerosis. However, the precise role of X-inactive-specific transcript (XIST) in atherosclerosis remains unclear. The proliferation and apoptosis of human umbilical vein endothelial cells (HUVECs) exposed to low-density lipoprotein (ox-LDL) were assessed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazol-3-ium bromide, and flow cytometry assays, correspondingly. The western blot assay was used to quantify protein expression. Lactate dehydrogenase activity and the concentrations of inflammatory factors were measured by matched kits. The real-time quantitative polymerase chain reaction (qPCR) was used to determine α-smooth muscle actin, smooth muscle protein 22-α, XIST, miR-98-5p, and pregnancy-associated plasma protein A (PAPPA) levels in HUVECs. The relationship among XIST, miR-98-5p, and PAPPA was analyzed by dual-luciferase reporter, RNA immunoprecipitation, and RNA pull-down assays. We found ox-LDL repressed proliferation and induced inflammation and apoptosis in HUVECs. Loss-of-functional experiment suggested that the downregulation of XIST overturned the ox-LDL-induced effects on HUVECs. Additionally, overexpression of miR-98-5p-induced effects on ox-LDL-stimulated HUVECs was abolished by upregulation of XIST. However, silencing of miR-98-5p strengthened the ox-LDL-induced effects on HUVECs by increasing expression of PAPPA. Mechanistically, XIST could regulate PAPPA expression in ox-LDL-induced HUVECs by sponging miR-98-5p, providing understanding for atherosclerosis.
format	article
author	Gao Hongmei Guo Zhaohui
author_facet	Gao Hongmei Guo Zhaohui
author_sort	Gao Hongmei
title	LncRNA XIST regulates atherosclerosis progression in ox-LDL-induced HUVECs
title_short	LncRNA XIST regulates atherosclerosis progression in ox-LDL-induced HUVECs
title_full	LncRNA XIST regulates atherosclerosis progression in ox-LDL-induced HUVECs
title_fullStr	LncRNA XIST regulates atherosclerosis progression in ox-LDL-induced HUVECs
title_full_unstemmed	LncRNA XIST regulates atherosclerosis progression in ox-LDL-induced HUVECs
title_sort	lncrna xist regulates atherosclerosis progression in ox-ldl-induced huvecs
publisher	De Gruyter
publishDate	2021
url	https://doaj.org/article/59efd9ddd39c46b5b28c3ea6ac1f0e90
work_keys_str_mv	AT gaohongmei lncrnaxistregulatesatherosclerosisprogressioninoxldlinducedhuvecs AT guozhaohui lncrnaxistregulatesatherosclerosisprogressioninoxldlinducedhuvecs
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LncRNA XIST regulates atherosclerosis progression in ox-LDL-induced HUVECs

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