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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Main Authors: Bian Yuan, Cai Wenqiang, Lu Hongying, Tang Shuhong, Yang Keqin, Tan Yan
Format: Article
Language:English
Published: De Gruyter 2021-11-01
Series:Open Medicine
Subjects:
Online Access:https://doi.org/10.1515/med-2021-0357
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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
collection DOAJ
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.
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spelling doaj.art-ba9640c4da1748fda20489914f1afe342022-12-22T04:28:59ZengDe GruyterOpen Medicine2391-54632021-11-011611642165210.1515/med-2021-0357miR-150-5p affects AS plaque with ASMC proliferation and migration by STAT1Bian Yuan0Cai Wenqiang1Lu Hongying2Tang Shuhong3Yang Keqin4Tan Yan5Department of Neurosurgery, Guigang City People’s Hospital, Guigang, 537100, ChinaDepartment of Neurosurgery, Guigang City People’s Hospital, Guigang, 537100, ChinaDepartment of Neurosurgery, Guigang City People’s Hospital, Guigang, 537100, ChinaDepartment of Neurosurgery, Guigang City People’s Hospital, Guigang, 537100, ChinaDepartment of Neurosurgery, Guigang City People’s Hospital, Guigang, 537100, ChinaDepartment of Neurosurgery, Guigang City People’s Hospital, No. 1, Zhongshan Middle Road, Guigang, 537100, ChinaWe 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.https://doi.org/10.1515/med-2021-0357atherosclerosismir-150-5pplaque stabilitycollagen metabolismsignal transducer and activator of transcription 1
spellingShingle 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
Open Medicine
atherosclerosis
mir-150-5p
plaque stability
collagen metabolism
signal transducer and activator of transcription 1
title 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_short 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
topic atherosclerosis
mir-150-5p
plaque stability
collagen metabolism
signal transducer and activator of transcription 1
url https://doi.org/10.1515/med-2021-0357
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AT luhongying mir1505paffectsasplaquewithasmcproliferationandmigrationbystat1
AT tangshuhong mir1505paffectsasplaquewithasmcproliferationandmigrationbystat1
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