LncRNA NEAT1 Promote Inflammatory Responses in Coronary Slow Flow Through Regulating miR-148b-3p/ICAM-1 Axis

Qing Zhu,1 Cuiting Zhao,1 Yonghuai Wang,1 Xinxin Li,1 Yixue Xue,2– 4 Chunyan Ma1 1Department of Cardiovascular Ultrasound, The First Hospital of China Medical University, Shenyang, People’s Republic of China; 2Department of Neurobiology, School of Life Sciences, China Medical Uni...

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Autores principales:	Zhu Q, Zhao C, Wang Y, Li X, Xue Y, Ma C
Formato:	article
Lenguaje:	EN
Publicado:	Dove Medical Press 2021
Materias:	coronary slow flow ncrna inflammation biomarkers cell biology Pathology RB1-214 Therapeutics. Pharmacology RM1-950
Acceso en línea:	https://doaj.org/article/63744ba588554f6493cfeca52ffa8a20
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spelling	oai:doaj.org-article:63744ba588554f6493cfeca52ffa8a202021-12-02T15:04:11ZLncRNA NEAT1 Promote Inflammatory Responses in Coronary Slow Flow Through Regulating miR-148b-3p/ICAM-1 Axis1178-7031https://doaj.org/article/63744ba588554f6493cfeca52ffa8a202021-06-01T00:00:00Zhttps://www.dovepress.com/lncrna-neat1-promote-inflammatory-responses-in-coronary-slow-flow-thro-peer-reviewed-fulltext-article-JIRhttps://doaj.org/toc/1178-7031Qing Zhu,1 Cuiting Zhao,1 Yonghuai Wang,1 Xinxin Li,1 Yixue Xue,2– 4 Chunyan Ma1 1Department of Cardiovascular Ultrasound, The First Hospital of China Medical University, Shenyang, People’s Republic of China; 2Department of Neurobiology, School of Life Sciences, China Medical University, Shenyang, People’s Republic of China; 3Key Laboratory of Cell Biology, Ministry of Public Health of China, China Medical University, Shenyang, People’s Republic of China; 4Key Laboratory of Medical Cell Biology, Ministry of Education of China, China Medical University, Shenyang, People’s Republic of ChinaCorrespondence: Chunyan MaDepartment of Cardiovascular Ultrasound, The First Hospital of China Medical University, No. 155 Nanjingbei Street, Shenyang, Liaoning, 110001, People’s Republic of ChinaTel +86 2483282129Email cmu1h_mcy@126.comBackground: Coronary slow flow (CSF) is an angiographic phenomenon characterized by delayed coronary opacification with normal or near-normal epicardial coronary arteries. The pathogenesis of CSF is closely related to inflammatory response. Accumulating evidence shows that long non-coding RNAs (lncRNAs) play an important role in cardiovascular disease. However, the mechanism underlying the influence of the lncRNA nuclear enriched abundant transcripts 1 (NEAT1) on CSF is still unknown.Patients and Methods: Forty CSF patients and forty control subjects were included in the study and underwent coronary angiography, Seattle angina questionnaire (SAQ) and echocardiography. The plasma levels of the inflammatory factors soluble intercellular adhesion molecule-1 (sICAM-1), interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-α) were determined by ELISA. The expression levels of NEAT1, miR-148b-3p and ICAM-1 in cells were measured by qRT-PCR or Western blotting. Cell proliferation was measured by 5‐Ethynyl‐2ʹ‐deoxyuridine (EdU) and Cell Counting Kit-8 (CCK-8) assay. Cell apoptosis was detected by apoptosis assay. The relationship between NEAT1 and miR-148b-3p was verified by luciferase reporter gene assay, RNA immunoprecipitation (RIP) assay and avidin-biotin pull-down assay. The relationship between ICAM-1 and miR-148b-3p was verified by luciferase reporter gene assay and avidin-biotin pull-down assay.Results: This study showed that plasma sICAM-1, miR-148b-3p, and NEAT1 as independent predictors of a CSF diagnosis. Furthermore, plasma NEAT1 level showed superior diagnostic ability for CSF compared with sICAM-1 and miR-148b-3p. It was also shown that high expression of NEAT1 in oxygen-glucose deprivation (OGD)-treated human umbilical vein endothelial cells (HUVECs) functions as a competing endogenous RNA (ceRNA). By specifically binding miR-148b-3p, it weakened the negative regulatory effects of miR-148b-3p on the ICAM-1 target gene leading to upregulated expression of ICAM-1. This interaction was also shown to inhibit HUVEC proliferation and enhance apoptosis.Conclusion: This study demonstrated for the first time the important mechanism of action of the NEAT1/miR-148b-3p/ICAM-1 axis in the progression of CSF disease, and indicated the potential of NEAT1, miR-148b-3p, and ICAM-1 as a new target for the diagnosis and treatment of CSF.Keywords: coronary slow flow, ncRNA, inflammation, biomarkers, cell biologyZhu QZhao CWang YLi XXue YMa CDove Medical Pressarticlecoronary slow flowncrnainflammationbiomarkerscell biologyPathologyRB1-214Therapeutics. PharmacologyRM1-950ENJournal of Inflammation Research, Vol Volume 14, Pp 2445-2463 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	coronary slow flow ncrna inflammation biomarkers cell biology Pathology RB1-214 Therapeutics. Pharmacology RM1-950
spellingShingle	coronary slow flow ncrna inflammation biomarkers cell biology Pathology RB1-214 Therapeutics. Pharmacology RM1-950 Zhu Q Zhao C Wang Y Li X Xue Y Ma C LncRNA NEAT1 Promote Inflammatory Responses in Coronary Slow Flow Through Regulating miR-148b-3p/ICAM-1 Axis
description	Qing Zhu,1 Cuiting Zhao,1 Yonghuai Wang,1 Xinxin Li,1 Yixue Xue,2– 4 Chunyan Ma1 1Department of Cardiovascular Ultrasound, The First Hospital of China Medical University, Shenyang, People’s Republic of China; 2Department of Neurobiology, School of Life Sciences, China Medical University, Shenyang, People’s Republic of China; 3Key Laboratory of Cell Biology, Ministry of Public Health of China, China Medical University, Shenyang, People’s Republic of China; 4Key Laboratory of Medical Cell Biology, Ministry of Education of China, China Medical University, Shenyang, People’s Republic of ChinaCorrespondence: Chunyan MaDepartment of Cardiovascular Ultrasound, The First Hospital of China Medical University, No. 155 Nanjingbei Street, Shenyang, Liaoning, 110001, People’s Republic of ChinaTel +86 2483282129Email cmu1h_mcy@126.comBackground: Coronary slow flow (CSF) is an angiographic phenomenon characterized by delayed coronary opacification with normal or near-normal epicardial coronary arteries. The pathogenesis of CSF is closely related to inflammatory response. Accumulating evidence shows that long non-coding RNAs (lncRNAs) play an important role in cardiovascular disease. However, the mechanism underlying the influence of the lncRNA nuclear enriched abundant transcripts 1 (NEAT1) on CSF is still unknown.Patients and Methods: Forty CSF patients and forty control subjects were included in the study and underwent coronary angiography, Seattle angina questionnaire (SAQ) and echocardiography. The plasma levels of the inflammatory factors soluble intercellular adhesion molecule-1 (sICAM-1), interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-α) were determined by ELISA. The expression levels of NEAT1, miR-148b-3p and ICAM-1 in cells were measured by qRT-PCR or Western blotting. Cell proliferation was measured by 5‐Ethynyl‐2ʹ‐deoxyuridine (EdU) and Cell Counting Kit-8 (CCK-8) assay. Cell apoptosis was detected by apoptosis assay. The relationship between NEAT1 and miR-148b-3p was verified by luciferase reporter gene assay, RNA immunoprecipitation (RIP) assay and avidin-biotin pull-down assay. The relationship between ICAM-1 and miR-148b-3p was verified by luciferase reporter gene assay and avidin-biotin pull-down assay.Results: This study showed that plasma sICAM-1, miR-148b-3p, and NEAT1 as independent predictors of a CSF diagnosis. Furthermore, plasma NEAT1 level showed superior diagnostic ability for CSF compared with sICAM-1 and miR-148b-3p. It was also shown that high expression of NEAT1 in oxygen-glucose deprivation (OGD)-treated human umbilical vein endothelial cells (HUVECs) functions as a competing endogenous RNA (ceRNA). By specifically binding miR-148b-3p, it weakened the negative regulatory effects of miR-148b-3p on the ICAM-1 target gene leading to upregulated expression of ICAM-1. This interaction was also shown to inhibit HUVEC proliferation and enhance apoptosis.Conclusion: This study demonstrated for the first time the important mechanism of action of the NEAT1/miR-148b-3p/ICAM-1 axis in the progression of CSF disease, and indicated the potential of NEAT1, miR-148b-3p, and ICAM-1 as a new target for the diagnosis and treatment of CSF.Keywords: coronary slow flow, ncRNA, inflammation, biomarkers, cell biology
format	article
author	Zhu Q Zhao C Wang Y Li X Xue Y Ma C
author_facet	Zhu Q Zhao C Wang Y Li X Xue Y Ma C
author_sort	Zhu Q
title	LncRNA NEAT1 Promote Inflammatory Responses in Coronary Slow Flow Through Regulating miR-148b-3p/ICAM-1 Axis
title_short	LncRNA NEAT1 Promote Inflammatory Responses in Coronary Slow Flow Through Regulating miR-148b-3p/ICAM-1 Axis
title_full	LncRNA NEAT1 Promote Inflammatory Responses in Coronary Slow Flow Through Regulating miR-148b-3p/ICAM-1 Axis
title_fullStr	LncRNA NEAT1 Promote Inflammatory Responses in Coronary Slow Flow Through Regulating miR-148b-3p/ICAM-1 Axis
title_full_unstemmed	LncRNA NEAT1 Promote Inflammatory Responses in Coronary Slow Flow Through Regulating miR-148b-3p/ICAM-1 Axis
title_sort	lncrna neat1 promote inflammatory responses in coronary slow flow through regulating mir-148b-3p/icam-1 axis
publisher	Dove Medical Press
publishDate	2021
url	https://doaj.org/article/63744ba588554f6493cfeca52ffa8a20
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LncRNA NEAT1 Promote Inflammatory Responses in Coronary Slow Flow Through Regulating miR-148b-3p/ICAM-1 Axis

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