Abstract 316: Salusin-α Improved Atherosclerosis in High Cholesterol Diet Fed Rabbits by Inhibiting Smooth Muscle Cells Proliferation and Migration

2018 ◽  
Vol 123 (Suppl_1) ◽  
Author(s):  
Gao Shoucui ◽  
Wang Xiaojing ◽  
Zhao Sihai ◽  
Fan Jianglin ◽  
Liu Enqi
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
High Cholesterol Diet ◽  
Cholesterol Diet ◽  
High Cholesterol ◽  
And Migration ◽  
Proliferation And Migration

SHORT TERM HIGH CHOLESTEROL DIET CAUSES CHANGES IN MEGAKARYOCYTE SIZE AND IN VASCULAR ULTRASTRUCTURE

1987 ◽  
Author(s):  
S Dalby Kristensen ◽  
K M Roberts ◽  
J Lawry ◽  
J F Martin
Keyword(s):  
Smooth Muscle ◽  
Normal Diet ◽  
High Cholesterol Diet ◽  
Cholesterol Diet ◽  
High Cholesterol ◽  
Short Term ◽  
Transmission Electron ◽  
Perfusion Fixation ◽  
And Migration ◽  
Proliferation And Migration

Platelets produced by megakaryocytes (MK) have a role in atherogenesis. Six pairs of male litter mate rabbits were randomised to feeding with either 2g of cholesterol daily in addition to their normal diet or normal diet alone. After seven days the animals were killed and serum cholesterol, platelet count, MK total, cytoplasmic and nuclear area (microscopic planimetry) and MK DNA content cell distribution (fluorescent activated cell sorting) were measured and compared between the two groups. The results are given in the table as medians with range values in brackets.After perfusion-fixation the aortas were examined by transmission electron microscopy. In the aortas from the animals on high cholesterol diet cells with ultrastructural features resembling smooth muscle cells were found in the intima. Changes in megakaryocyte size are associated with the occurrence of smooth muscle cell proliferation and migration. The platelet-megakaryocyte axis may be activated in early atherogenesis.

Abstract 279: Vitamin D3 Attenuates ADAM-12--Mediated Shedding of EGFR in Carotid Artery Smooth Muscle Cells of Hypercholesterolemic Swine

2012 ◽  
Vol 32 (suppl_1) ◽  
Author(s):  
Vikash Kansal ◽  
Swastika Sur ◽  
Velidi H Rao ◽  
Devendra K Agrawal
Keyword(s):  
Vitamin D ◽  
Cell Proliferation ◽  
Smooth Muscle ◽  
Carotid Artery ◽  
Smooth Muscle Cells ◽  
High Cholesterol Diet ◽  
Cholesterol Diet ◽  
High Cholesterol ◽  
Mrna Transcripts ◽  
Adam 12

Deficiency of Vitamin D is linked to an increased risk of hypertension, peripheral artery disease, and myocardial infarction and is a major risk factor for the development of human atherosclerosis. Atheromatous cytokines, including TNF-α, IL-6 and IFN-γ, and EGF receptor family growth factors are released at the site of atherosclerosis and act on proteolytic enzymes, MMPs (matrix metalloproteinases), ADAMs (a disintegrin and metalloproteinases), and ADAMTS (a disintegrin and metalloproteinase with thrombospondin motifs). ADAM-12 activates EGFR resulting in increased migration and proliferation of smooth muscle cells (SMCs). The aim of this study was to examine the effect of vitamin D on IL-6-induced ADAM-12 expression and SMC migration and proliferation. Micro-swine were fed with either vitamin D-deficient high cholesterol diet or high cholesterol diet containing 900 IU of vitamin D for 6 months. After six months when serum cholesterol levels ranged from 500-600 mg/dL, vitamin D-deficient group continued on the same deficient diet, whereas the other group received supplementation of vitamin D (1,000 IU/d) for 6 months. The mRNA expression of ADAM-12 and EGFR in whole carotid artery and in IL-6-treated SMCs was quantified by qPCR. The proliferation was assayed by CyQuant NF cell proliferation assay. The mRNA transcripts of ADAM-12 and EGFR were significantly increased in carotid arteries from Vitamin D-deficient than in vitamin D- supplemented swine. Treatment of SMCs with IL-6 also increased the mRNA transcripts of ADAM-12 and EGFR in vitamin D-deficient swine SMCs compared to vitamin D-supplemented swine SMCs. The cell proliferation was higher in SMCs isolated from Vitamin D-deficient swine carotid artery compared to vitamin D- supplemented swine carotid artery. Together, these results suggest that Vitamin D regulates ADAM-12-mediated activation of EGFR and vitamin D deficiency further enhances proliferation of SMCs, which is potentiated by atheromatous cytokines.

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 PDGFBB promotes proliferation and migration via regulating miR-1181/STAT3 axis in human pulmonary arterial smooth muscle cells

2018 ◽  
Vol 315 (6) ◽  
pp. L965-L976 ◽  
Author(s):  
Zhengjiang Qian ◽  
Yanjiao Li ◽  
Haiyang Yang ◽  
Jidong Chen ◽  
Xiang Li ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Causative Factor ◽  
Loss Of Function ◽  
Migration Flow ◽  
Pulmonary Arterial ◽  
And Migration ◽  
Proliferation And Migration

Platelet-derived growth factor (PDGF) can induce hyperproliferation of pulmonary artery smooth muscle cells (PASMCs), which is a key causative factor to the occurrence and progression of pulmonary arterial hypertension (PAH). We previously identified that miR-1181 is significantly downregulated by PDGFBB in human PASMCs. In this work, we further explore the function of miR-1181 and underlying regulatory mechanisms in PDGF-induced PASMCs. First, the expression pattern of miR-1181 was characterized under PDGFBB treatment, and PDGF receptor/PKCβ signaling was found to repress miR-1181 expression. Then, gain- and loss-of-function experiments were respectively conducted and revealed the prominent role of miR-1181 in inhibiting PASMC proliferation and migration. Flow cytometry analysis suggested that miR-1181 regulated the PASMC proliferation through influencing the cell cycle transition from G0/G1 to S phase. Moreover, we exhibited that miR-1181 targeting STAT3 formed a regulatory axis to modulate PASMC proliferation. Finally, serum miR-1181 expression was also observed to be reduced in adult and newborn patients with PAH. Overall, this study provides novel findings that the miR-1181/STAT3 axis mediated PDGFBB-induced dysfunction in human PASMCs, implying a potential use of miR-1181 as a therapeutic and diagnostic candidate for the vascular remodeling diseases.

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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