miR-33a-5p Inhibits the Proliferation and Migration of Vascular Smooth Muscle Cells in Atherosclerosis by Targeting S1PR1

2019 ◽  
Vol 9 (7) ◽  
pp. 943-949
Author(s):  
Jiong Li ◽  
Ning Xie ◽  
Yanzhen Wang ◽  
Yirong Gan ◽  
Zongke Kou ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Luciferase Reporter ◽  
Promote Cell Proliferation ◽  
Invasion And Migration ◽  
Arterial Walls ◽  
And Migration

Background: Atherosclerosis is determined as a chronic, complicated disease, and arterial walls were mainly composed of vascular smooth muscle cells (VSMCs). microRNAs (miRNAs) have been consistently demonstrated to be involved in VSMCs, and miR-33a-5p was reported concerning many biological functions of cells. However, the role of miR-33a-5p during atherosclerosis still unclear. Methods: In present study, human VSMCs were treated with platelet-derived growth factorbb (PDGF-bb) after transfection. The miR-33a-5p and S1PR1 expression levels were determined by qRT-PCR and/or Western blot assays. VSMCs proliferation, invasion and migration were measured by CCK-8, transwell and wound healing assays, respectively. Luciferase reporter assay was employed to validate the direct targeting of S1PR1 by miR-33a-5p. Results: The results showed that PDGF-bb treated after 24 h could promote cell proliferation and regulate the expression of miR-33a-5p and S1PR1 in VSMCs. Overexpression of miR-33a-5p inhibited proliferation, invasion and migration in PDGF-bb treated VSMCs. Furthermore, we proved that miR-33a-5p could directly target S1PR1, and miR-33a-5p mimic suppressed the expression of S1PR1 in PDGF-bb treated VSMCs. Conclusions: The results suggested that miR-33a-5p could inhibit the proliferation, invasion and migration of VSMCs via suppressed the expression of S1PR1. miR-33a-5p/S1PR1 axis may represent a potential therapeutic strategy to improve atherosclerosis.

scholarly journals LncRNA SNHG12 promotes proliferation and migration of vascular smooth muscle cells via targeting miR-766-5p/ EIF5A

2020 ◽  
Author(s):  
wen liu ◽  
jianhuan che ◽  
Yan Gu ◽  
ling song ◽  
yingying Jiao ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Translation Initiation Factor ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
And Migration ◽  
Proliferation And Migration

Abstract Background Although lncRNAs have reported to serve as potential biomarkers of atherosclerosis (AS), the role of lncRNA SNHG12 in AS are still unknown. Methods In present study, we investigated the regulatory effects of SNHG12 on human vascular smooth muscle cells (hVSMCs). RT-qPCR were employed to determine the expressions of SNHG12, miR-766-5p and eukaryotic translation initiation factor 5A (EIF5A). Cell viability was estimated via the Cell Counting Kit-8 assay. Wound healing and Transwell invasion assays were used for evaluation of hVSMCs migratory capacity. To further investigate the regulatory mechanisms, binding sites between SNHG12 and miR-766-5p, EIF5A and miR-766-5p were speculated via starBase V2.0, and validated using luciferase reporter gene assay. Results It was identified that SNHG12 was up-regulated in oxidized low-density lipoprotein (ox-LDL)-insulted hVSMCs. Silencing SNHG12 inhibited ox-LDL-induced proliferation and migration of hVSMCs. Moreover, we found that SNHG12 acted as a sponge of miR-766-5p, and miR-766-5p also interacted with EIF5A. EIF5A plasmids promoted the proliferation and migratory capacities of hVSMCs, however, shRNA-SNHG12 counteracted the facilitation of EIF5A plasmids on biological behaviors of hVSMCs. Conclusions These findings of this study demonstrated that SNHG12 facilitated the migration and invasion of hVSMCs via targeting miR-766-5p/EIF5A axis.

MiR-506-3p Promotes the Proliferation and Migration of Vascular Smooth Muscle Cells via Targeting KLF4

Pathobiology ◽  
2021 ◽  
pp. 1-12
Author(s):  
Hang Dong ◽  
Guangyu Jiang ◽  
Jiayue Zhang ◽  
Yuming Kang
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Qrt Pcr ◽  
And Migration ◽  
Proliferation And Migration

<b><i>Background:</i></b> The dysregulation of proliferation and migration of vascular smooth muscle cells (VSMCs) is one of the major causes of atherosclerosis (AS). Accumulating studies confirm that Kruppel-like factor 4 (KLF4) can regulate the proliferation and differentiation of VSMCs through multiple signaling pathways. However, the mechanism of KLF4 dysregulation remains unknown. <b><i>Methods:</i></b> Apolipoprotein E-knockout (ApoE<sup>−/−</sup>) mice and human VSMCs were used to establish AS animal model and cell model, respectively. qRT-PCR was employed to determine the expressions of miR-506-3p and KLF4. Cell Counting Kit -8, Transwell, TUNEL assays, and flow cytometry were performed to measure the proliferation, migration, and apoptosis of VSMCs. The upstream miRNAs of KLF4 were predicted by microT, miRanda, miRmap, and TargetScan databases. The interaction between KLF4 and miR-506-3p was confirmed using qRT-PCR, Western blot, and luciferase reporter gene assay. <b><i>Results:</i></b> KLF4 expression was significantly decreased in the VSMCs of ApoE<sup>−/−</sup> mice fed with high-fat diet and in human VSMCs treated with oxidized low-density lipoprotein in time-dependent and dose-dependent manners. The transfection of miR-506-3p mimics or KLF4 shRNA promoted the proliferation and migration of VSMCs but inhibited the apoptosis while miR-506-3p inhibitors and pcDNA3.1-KLF4 exerted opposite effects. Additionally, KLF4 was confirmed as a target gene of miR-506-3p and could be negatively regulated by miR-506-3p. <b><i>Conclusion:</i></b> MiR-506-3p can promote the proliferation and migration of VSMCs via targeting KLF4, which can probably contribute to the pathogenesis of AS.

Circ-CHFR modulates the proliferation, migration, and invasion of ox-LDL-induced human aorta vascular smooth muscle cells through the miR-214-3p/PAPPA axis

2021 ◽  
pp. 1-14
Author(s):  
Qianqian Lu ◽  
Ying Li ◽  
Jiaping Lou ◽  
Pingzhen Li ◽  
Yi Gu ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Quantitative Polymerase Chain Reaction ◽  
Muscle Cells ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Circular Rnas ◽  
Human Aorta

Circular RNAs (circRNAs) are associated with the pathogenesis of human diseases, including atherosclerosis. Here, we undertook to investigate the biological role and mechanism of circRNA E3 ubiquitin-protein ligase (circ-CHFR) in atherosclerosis. The expression levels of circ-CHFR, miR-214-3p, and pregnancy-associated plasma protein A (PAPPA) were measured by real-time quantitative polymerase chain reaction (RT-qPCR) and western blot in human aorta vascular smooth muscle cells (HA-VSMCs) exposed to oxidized low-density lipoprotein (ox-LDL). Cell proliferation, migration, and invasion capabilities were assessed by 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyl-2H-tetrazol-3-ium bromide (MTT), and transwell assays, respectively. The relationship between miR-214-3p and circ-CHFR or PAPPA was confirmed by dual-luciferase reporter and RNA immunoprecipitation (RIP) assays. Our data showed that circ-CHFR was upregulated in HA-VSMCs after stimulation with ox-LDL. Downregulation of circ-CHFR inhibited the proliferation, migration, and invasion of HA-VSMCs exposed to ox-LDL. Mechanistically, circ-CHFR acted as a miR-214-3p sponge, and miR-214-3p was a molecular mediator of circ-CHFR regulation in ox-LDL-stimulated HA-VSMCs. PAPPA was a miR-214-3p target, and circ-CHFR regulated the expression of PAPPA by sponging miR-214-3p. Moreover, overexpression of miR-214-3p repressed the proliferation, migration, and invasion of ox-LDL-induced HA-VSMCs by decreasing PAPPA expression. Our findings suggest that the circ-CHFR/miR-214-3p/PAPPA axis regulates ox-LDL-induced proliferation, migration, and invasion in HA-VSMCs.

RNAi-mediated Rab5a suppression inhibits proliferation and migration of vascular smooth muscle cells

2010 ◽  
Vol 65 (5) ◽  
pp. 507-514 ◽  
Author(s):  
Zhigang Ma ◽  
Hao Wang ◽  
Liang Wu ◽  
Lei Zhu ◽  
Weihao Shi ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
And Migration ◽  
Proliferation And Migration
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