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Liraglutide blocks the proliferation, migration and phenotypic switching of Homocysteine (Hcy)-induced vascular smooth muscle cells (VSMCs) by suppressing proprotein convertase subtilisin kexin9 (PCSK9)/ low-density lipoprotein receptor (LDLR)

Liraglutide, a glucagon-like peptide 1 (GLP1) receptor agonist, is known to inhibit the atherosclerosis of apoE mice and suppress the cellular behaviors of VSMCs induced by AngII. This study aimed to explore whether liraglutide can reduce the proliferation, invasion and phenotypic transformation of...

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Detalles Bibliográficos
Autores principales: Ji, Jingquan, Feng, Ming, Niu, Xiaohong, Zhang, Xinyu, Wang, Yilei
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Taylor & Francis 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8806487/
https://www.ncbi.nlm.nih.gov/pubmed/34666623
http://dx.doi.org/10.1080/21655979.2021.1982304
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author Ji, Jingquan
Feng, Ming
Niu, Xiaohong
Zhang, Xinyu
Wang, Yilei
author_facet Ji, Jingquan
Feng, Ming
Niu, Xiaohong
Zhang, Xinyu
Wang, Yilei
author_sort Ji, Jingquan
collection PubMed
description Liraglutide, a glucagon-like peptide 1 (GLP1) receptor agonist, is known to inhibit the atherosclerosis of apoE mice and suppress the cellular behaviors of VSMCs induced by AngII. This study aimed to explore whether liraglutide can reduce the proliferation, invasion and phenotypic transformation of VSMCs induced by Hcy and the underlying mechanism. Hcy was used to induce the proliferation of VSMCs, and liraglutide was then used to expose the cells for assessing cell proliferation. Afterward, the cell migration and phenotypic switch were evaluated to observe the effects of liraglutide. Meanwhile, the expression of PCSK9 and LDLR was detected. After overexpressing PCSK9, the changes in proliferation, cell migration and phenotypic switch were estimated again. Hcy promoted cell proliferation of VSMCs, whereas liraglutide blocked the proliferation, migration and phenotypic switch of Hcy-induced VSMCs. Furthermore, the expression of PCSK9 was downregulated and LDLR expression was upregulated after liraglutide administration in Hcy-induced VSMCs. After overexpressing PCSK9, the proliferation, migration and phenotypic switch of Hcy-induced VSMCs were enhanced. Liraglutide blocked the proliferation, migration and phenotypic switching of Hcy-induced VSMCs by suppressing PCSK9/LDLR. This finding provided the basis for the future application of liraglutide as an effective drug for therapeutic strategy in targeting AS.
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spelling pubmed-88064872022-02-02 Liraglutide blocks the proliferation, migration and phenotypic switching of Homocysteine (Hcy)-induced vascular smooth muscle cells (VSMCs) by suppressing proprotein convertase subtilisin kexin9 (PCSK9)/ low-density lipoprotein receptor (LDLR) Ji, Jingquan Feng, Ming Niu, Xiaohong Zhang, Xinyu Wang, Yilei Bioengineered Research Paper Liraglutide, a glucagon-like peptide 1 (GLP1) receptor agonist, is known to inhibit the atherosclerosis of apoE mice and suppress the cellular behaviors of VSMCs induced by AngII. This study aimed to explore whether liraglutide can reduce the proliferation, invasion and phenotypic transformation of VSMCs induced by Hcy and the underlying mechanism. Hcy was used to induce the proliferation of VSMCs, and liraglutide was then used to expose the cells for assessing cell proliferation. Afterward, the cell migration and phenotypic switch were evaluated to observe the effects of liraglutide. Meanwhile, the expression of PCSK9 and LDLR was detected. After overexpressing PCSK9, the changes in proliferation, cell migration and phenotypic switch were estimated again. Hcy promoted cell proliferation of VSMCs, whereas liraglutide blocked the proliferation, migration and phenotypic switch of Hcy-induced VSMCs. Furthermore, the expression of PCSK9 was downregulated and LDLR expression was upregulated after liraglutide administration in Hcy-induced VSMCs. After overexpressing PCSK9, the proliferation, migration and phenotypic switch of Hcy-induced VSMCs were enhanced. Liraglutide blocked the proliferation, migration and phenotypic switching of Hcy-induced VSMCs by suppressing PCSK9/LDLR. This finding provided the basis for the future application of liraglutide as an effective drug for therapeutic strategy in targeting AS. Taylor & Francis 2021-10-19 /pmc/articles/PMC8806487/ /pubmed/34666623 http://dx.doi.org/10.1080/21655979.2021.1982304 Text en © 2021 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group. https://creativecommons.org/licenses/by/4.0/This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Paper
Ji, Jingquan
Feng, Ming
Niu, Xiaohong
Zhang, Xinyu
Wang, Yilei
Liraglutide blocks the proliferation, migration and phenotypic switching of Homocysteine (Hcy)-induced vascular smooth muscle cells (VSMCs) by suppressing proprotein convertase subtilisin kexin9 (PCSK9)/ low-density lipoprotein receptor (LDLR)
title Liraglutide blocks the proliferation, migration and phenotypic switching of Homocysteine (Hcy)-induced vascular smooth muscle cells (VSMCs) by suppressing proprotein convertase subtilisin kexin9 (PCSK9)/ low-density lipoprotein receptor (LDLR)
title_full Liraglutide blocks the proliferation, migration and phenotypic switching of Homocysteine (Hcy)-induced vascular smooth muscle cells (VSMCs) by suppressing proprotein convertase subtilisin kexin9 (PCSK9)/ low-density lipoprotein receptor (LDLR)
title_fullStr Liraglutide blocks the proliferation, migration and phenotypic switching of Homocysteine (Hcy)-induced vascular smooth muscle cells (VSMCs) by suppressing proprotein convertase subtilisin kexin9 (PCSK9)/ low-density lipoprotein receptor (LDLR)
title_full_unstemmed Liraglutide blocks the proliferation, migration and phenotypic switching of Homocysteine (Hcy)-induced vascular smooth muscle cells (VSMCs) by suppressing proprotein convertase subtilisin kexin9 (PCSK9)/ low-density lipoprotein receptor (LDLR)
title_short Liraglutide blocks the proliferation, migration and phenotypic switching of Homocysteine (Hcy)-induced vascular smooth muscle cells (VSMCs) by suppressing proprotein convertase subtilisin kexin9 (PCSK9)/ low-density lipoprotein receptor (LDLR)
title_sort liraglutide blocks the proliferation, migration and phenotypic switching of homocysteine (hcy)-induced vascular smooth muscle cells (vsmcs) by suppressing proprotein convertase subtilisin kexin9 (pcsk9)/ low-density lipoprotein receptor (ldlr)
topic Research Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8806487/
https://www.ncbi.nlm.nih.gov/pubmed/34666623
http://dx.doi.org/10.1080/21655979.2021.1982304
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