scholarly journals TRIM7 promotes proliferation and migration of vascular smooth muscle cells in atherosclerosis through activating c‐Jun/AP‐1

IUBMB Life ◽  
2019 ◽  
Vol 72 (2) ◽  
pp. 247-258 ◽  
Author(s):  
Rongjing Ji ◽  
Yuanyuan Gu ◽  
Jing Zhang ◽  
Chuanyu Gao ◽  
Wanli Gao ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
And Migration ◽  
Proliferation And Migration

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.

Betulinic acid inhibits high glucose-induced vascular smooth muscle cells proliferation and migration

2010 ◽  
Vol 111 (6) ◽  
pp. 1501-1511 ◽  
Author(s):  
Jung Joo Yoon ◽  
Yun Jung Lee ◽  
Jin Sook Kim ◽  
Dae Gill Kang ◽  
Ho Sub Lee
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
High Glucose ◽  
Betulinic Acid ◽  
Muscle Cells ◽  
And Migration ◽  
Proliferation And Migration

CEMIP regulates the proliferation and migration of vascular smooth muscle cells in atherosclerosis through the WNT–beta-catenin signaling pathway

2020 ◽  
Vol 98 (2) ◽  
pp. 249-257
Author(s):  
Qiang Xue ◽  
Xiaoli Wang ◽  
Xiaohui Deng ◽  
Yue Huang ◽  
Wei Tian
Keyword(s):  
Smooth Muscle ◽  
Cell Migration ◽  
Matrix Metalloproteinase ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Signaling Pathway ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
And Migration ◽  
Proliferation And Migration

In this study we investigated the regulatory role of cell-migration-inducing and hyaluronan-binding protein (CEMIP) in the proliferation and migration of vascular smooth muscle cells (VSMCs). The mRNA and protein levels of CEMIP were upregulated in the plasma samples from patients with atherosclerosis, and in VSMCs stimulated with platelet-derived growth factor-BB (PDGF-BB), compared with plasma from healthy subjects and untreated VSMCs. Silencing CEMIP suppressed PDGF-BB-induced cell migration and proliferation in VSMCs, as determined using a Cell Counting Kit-8 assays, 5-ethynyl-2′-deocyuridine (EDU) assays, flow cytometry, wound healing assays, and Transwell assays. Overexpression of CEMIP promoted the proliferation and migration of VSMCs via activation of the Wnt–β-catenin signaling pathway and the upregulation of its target genes, including matrix metalloproteinase-2, matrix metalloproteinase-7, cyclin D1, and c-myc, whereas CEMIP deficiency showed the opposite effects. The knockdown of CEMIP in ApoE−/− mice by intravenous injection of lentiviral vector expressing si-CEMIP protected against high-fat-diet-induced atherosclerosis, as shown by the reduced aortic lesion areas, aortic sinus lesion areas, and the concentration of blood lipids compared with mice normally expressing CEMIP. These results demonstrated that CEMIP regulates the proliferation and migration of VSMCs in atherosclerosis by activating the WNT–β-catenin signaling pathway, which suggests the therapeutic potential of CEMIP for the management of atherosclerosis.

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