scholarly journals miR-149-5p Inhibits Vascular Smooth Muscle Cells Proliferation, Invasion, and Migration by Targeting Histone Deacetylase 4 (HDAC4)

2019 ◽  
Vol 25 ◽  
pp. 7581-7590 ◽  
Author(s):  
Boya Zhang ◽  
Yang Dong ◽  
Ming Liu ◽  
Lei Yang ◽  
Zhuo Zhao
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Histone Deacetylase ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Invasion And Migration ◽  
Histone Deacetylase 4 ◽  
And Migration

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.

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

scholarly journals Jujuboside B Inhibits Neointimal Hyperplasia and Prevents Vascular Smooth Muscle Cell Dedifferentiation, Proliferation, and Migration via Activation of AMPK/PPAR-γ Signaling

2021 ◽  
Vol 12 ◽  
Author(s):  
Zaixiong Ji ◽  
Jiaqi Li ◽  
Jianbo Wang
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Neointimal Hyperplasia ◽  
Muscle Cells ◽  
Cell Dedifferentiation ◽  
Ppar Γ ◽  
And Migration ◽  
Proliferation And Migration

The uncontrolled proliferation and migration of vascular smooth muscle cells is a critical step in the pathological process of restenosis caused by vascular intimal hyperplasia. Jujuboside B (JB) is one of the main biologically active ingredients extracted from the seeds of Zizyphus jujuba (SZJ), which has the properties of anti-platelet aggregation and reducing vascular tension. However, its effects on restenosis after vascular intervention caused by VSMCs proliferation and migration remain still unknown. Herein, we present novel data showing that JB treatment could significantly reduce the neointimal hyperplasia of balloon-damaged blood vessels in Sprague-Dawley (SD) rats. In cultured VSMCs, JB pretreatment significantly reduced cell dedifferentiation, proliferation, and migration induced by platelet-derived growth factor-BB (PDGF-BB). JB attenuated autophagy and reactive oxygen species (ROS) production stimulated by PDGF-BB. Besides, JB promoted the phosphorylation of adenosine monophosphate-activated protein kinase (AMPK) and the expression of peroxisome proliferator-activated receptor-γ (PPAR-γ). Notably, inhibition of AMPK and PPAR-γ partially reversed the ability of JB to resist the proliferation and migration of VSMCs. Taken as a whole, our findings reveal for the first time the anti-restenosis properties of JB in vivo and in vitro after the endovascular intervention. JB antagonizes PDGF-BB-induced phenotypic switch, proliferation, and migration of vascular smooth muscle cells partly through AMPK/PPAR-γ pathway. These results indicate that JB might be a promising clinical candidate drug against in-stent restenosis, which provides a reference for further research on the prevention and treatment of vascular-related diseases.

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