miR-150-5p affects AS plaque with ASMC proliferation and migration by STAT1

We explore miR‐150‐5p in atherosclerosis (AS). The AS model was constructed using Apo E−/− mice with an injection of the miR-150-5p mimic or an inhibitor. Pathological characteristics were assessed using Oil red O staining and Masson staining. Quantitative reverse transcription-polymerase chain reac...

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Autores principales:	Bian Yuan, Cai Wenqiang, Lu Hongying, Tang Shuhong, Yang Keqin, Tan Yan
Formato:	article
Lenguaje:	EN
Publicado:	De Gruyter 2021
Materias:	atherosclerosis mir-150-5p plaque stability collagen metabolism signal transducer and activator of transcription 1 Medicine R
Acceso en línea:	https://doaj.org/article/ba9640c4da1748fda20489914f1afe34
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spelling	oai:doaj.org-article:ba9640c4da1748fda20489914f1afe342021-12-05T14:10:55ZmiR-150-5p affects AS plaque with ASMC proliferation and migration by STAT12391-546310.1515/med-2021-0357https://doaj.org/article/ba9640c4da1748fda20489914f1afe342021-11-01T00:00:00Zhttps://doi.org/10.1515/med-2021-0357https://doaj.org/toc/2391-5463We explore miR‐150‐5p in atherosclerosis (AS). The AS model was constructed using Apo E−/− mice with an injection of the miR-150-5p mimic or an inhibitor. Pathological characteristics were assessed using Oil red O staining and Masson staining. Quantitative reverse transcription-polymerase chain reaction (qRT-PCR) and Western blot were used to analyze the expressions of microRNA-150-5p (miR-150-5p), STAT1, α-SMA (α-smooth muscle actin) and proliferating cell nuclear antigen (PCNA). Targetscan and dual-luciferase reporter assay were used to analyze the interaction between miR-150-5p and STAT1. The viability, migration, cell cycle and α-SMA and PCNA expressions in oxidized low-density lipoprotein (ox-LDL)-stimulated primary human aortic smooth muscle cells (ASMCs) were assessed using molecular experiments. miR-150-5p was reduced in both AS mice and ox-LDL-stimulated human aortic smooth muscle cells but STAT1 had the opposite effect. The miR‐150‐5p inhibitor alleviated the increase of lipid plaque and reduced collagen accumulation in the aortas during AS. Upregulation of α-SMA and PCNA was reversed by miR-150-5p upregulation. STAT1 was targeted by miR‐150‐5p, and overexpressed miR-150-5p weakened the ox-LDL-induced increase of viability and migration abilities and blocked cell cycle in ASMCs, but overexpressed STAT1 blocked the effect of the miR‐150‐5p mimic. This paper demonstrates that miR-150-5p has potential as a therapeutic target in AS, with plaque stabilization by regulating ASMC proliferation and migration via STAT1.Bian YuanCai WenqiangLu HongyingTang ShuhongYang KeqinTan YanDe Gruyterarticleatherosclerosismir-150-5pplaque stabilitycollagen metabolismsignal transducer and activator of transcription 1MedicineRENOpen Medicine, Vol 16, Iss 1, Pp 1642-1652 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	atherosclerosis mir-150-5p plaque stability collagen metabolism signal transducer and activator of transcription 1 Medicine R
spellingShingle	atherosclerosis mir-150-5p plaque stability collagen metabolism signal transducer and activator of transcription 1 Medicine R Bian Yuan Cai Wenqiang Lu Hongying Tang Shuhong Yang Keqin Tan Yan miR-150-5p affects AS plaque with ASMC proliferation and migration by STAT1
description	We explore miR‐150‐5p in atherosclerosis (AS). The AS model was constructed using Apo E−/− mice with an injection of the miR-150-5p mimic or an inhibitor. Pathological characteristics were assessed using Oil red O staining and Masson staining. Quantitative reverse transcription-polymerase chain reaction (qRT-PCR) and Western blot were used to analyze the expressions of microRNA-150-5p (miR-150-5p), STAT1, α-SMA (α-smooth muscle actin) and proliferating cell nuclear antigen (PCNA). Targetscan and dual-luciferase reporter assay were used to analyze the interaction between miR-150-5p and STAT1. The viability, migration, cell cycle and α-SMA and PCNA expressions in oxidized low-density lipoprotein (ox-LDL)-stimulated primary human aortic smooth muscle cells (ASMCs) were assessed using molecular experiments. miR-150-5p was reduced in both AS mice and ox-LDL-stimulated human aortic smooth muscle cells but STAT1 had the opposite effect. The miR‐150‐5p inhibitor alleviated the increase of lipid plaque and reduced collagen accumulation in the aortas during AS. Upregulation of α-SMA and PCNA was reversed by miR-150-5p upregulation. STAT1 was targeted by miR‐150‐5p, and overexpressed miR-150-5p weakened the ox-LDL-induced increase of viability and migration abilities and blocked cell cycle in ASMCs, but overexpressed STAT1 blocked the effect of the miR‐150‐5p mimic. This paper demonstrates that miR-150-5p has potential as a therapeutic target in AS, with plaque stabilization by regulating ASMC proliferation and migration via STAT1.
format	article
author	Bian Yuan Cai Wenqiang Lu Hongying Tang Shuhong Yang Keqin Tan Yan
author_facet	Bian Yuan Cai Wenqiang Lu Hongying Tang Shuhong Yang Keqin Tan Yan
author_sort	Bian Yuan
title	miR-150-5p affects AS plaque with ASMC proliferation and migration by STAT1
title_short	miR-150-5p affects AS plaque with ASMC proliferation and migration by STAT1
title_full	miR-150-5p affects AS plaque with ASMC proliferation and migration by STAT1
title_fullStr	miR-150-5p affects AS plaque with ASMC proliferation and migration by STAT1
title_full_unstemmed	miR-150-5p affects AS plaque with ASMC proliferation and migration by STAT1
title_sort	mir-150-5p affects as plaque with asmc proliferation and migration by stat1
publisher	De Gruyter
publishDate	2021
url	https://doaj.org/article/ba9640c4da1748fda20489914f1afe34
work_keys_str_mv	AT bianyuan mir1505paffectsasplaquewithasmcproliferationandmigrationbystat1 AT caiwenqiang mir1505paffectsasplaquewithasmcproliferationandmigrationbystat1 AT luhongying mir1505paffectsasplaquewithasmcproliferationandmigrationbystat1 AT tangshuhong mir1505paffectsasplaquewithasmcproliferationandmigrationbystat1 AT yangkeqin mir1505paffectsasplaquewithasmcproliferationandmigrationbystat1 AT tanyan mir1505paffectsasplaquewithasmcproliferationandmigrationbystat1
_version_	1718371625131311104

miR-150-5p affects AS plaque with ASMC proliferation and migration by STAT1

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