The Effect of Local Alcohol Delivery in Reducing Intimal Hyperplasia Induced by Vascular Injury and the Clinical Implications

2004 ◽  
Vol 1 (1) ◽  
pp. 33-40
Author(s):  
Ming W. Liu
Keyword(s):  
Vascular Injury ◽  
Intimal Hyperplasia ◽  
Clinical Implications

Inhibition of Ras/ERK1/2 pathway contributes to the protective effect of Ginsenoside Re against intimal hyperplasia

2021 ◽  
Author(s):  
Chenying Gao ◽  
Kaina Zhang ◽  
Fanfan Liang ◽  
Wenzhuo Ma ◽  
Xixi Jiang ◽  
...  
Keyword(s):  
Protective Effect ◽  
Endovascular Treatment ◽  
Carotid Stenosis ◽  
Vascular Injury ◽  
Intimal Hyperplasia ◽  
Neointimal Hyperplasia ◽  
Ginsenoside Re ◽  
Term Efficacy

Neointimal hyperplasia is the major cause of carotid stenosis after vascular injury, which restricts the long-term efficacy of endovascular treatment and endarterectomy in preventing stenosis. Ginsenoside Re (Re) is a...

Abstract 169: Smad3 Drives Cross-Talk Between TGFß and Wnt/ß-Catenin Signaling Pathways in Smooth Muscle Cells

2014 ◽  
Vol 34 (suppl_1) ◽  
Author(s):  
Daniel M DiRenzo ◽  
Xu Dong Shi ◽  
Lian-Wang Guo ◽  
K Craig Kent
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Wnt Signaling ◽  
Vascular Injury ◽  
Cross Talk ◽  
Intimal Hyperplasia ◽  
Muscle Cells ◽  
Arterial Injury ◽  
Protein Levels ◽  
Qrt Pcr

Restenosis (neo-intimal hyperplasia) occurs in approximately 25-50% of patients undergoing arterial interventions, primarily due to the proliferation and migration of arterial smooth muscle cells (SMCs) into the peri-luminal area. Recently, Wnt/β-catenin signaling has been shown to promote SMC proliferation and enhance neo-intimal hyperplasia but its mechanism of activation is unclear. Interestingly, Wnt/β-catenin has been shown to be activated by TGFβ in mesenchymal stem cells and fibroblasts. We have shown that TGFβ and its downstream signaling protein, Smad3, are upregulated following vascular injury and that Smad3 overexpressing SMCs display enhanced proliferation, migration, and neo-intimal hyperplasia. These results led us to hypothesize that TGFβ, through Smad3, activates Wnt/β-catenin to regulate SMC behavior following arterial injury . In primary rat SMCs, TGFβ (5ng/mL) led to β-catenin activation and relocalization from the plasma membrane to the cytoplasm / nucleus within 24 hours. Furthermore, qRT-PCR results demonstrated that expression of Wnt11 (22 fold) and Wnt9a (3.9 fold) were significantly upregulated after 24 hours of TGFβ stimulation (p<0.05, n=3). In addition, 24 hours of TGFβ stimulation in SMCs overexpressing Smad3 (TGFβ/Smad3) further enhanced the gene expression of Wnt11 (>300 fold) and Wnt9a (14 fold) and also stimulated significant increases in Wnt2b (41 fold), Wnt5a (2.9 fold), and Wnt4 (3.2 fold) (p<0.05, n=3) as measured by qRT-PCR. Western blot results demonstrated that the combined TGFβ/Smad3 stimulation increased β-catenin protein levels, suggesting that TGFβ activates canonical Wnt signaling leading to stabilization of β-catenin protein. In normal rat carotid arteries, β-catenin protein was undetectable via immunohistochemistry but could be seen in SMCs of the vessel media at 3 days post-balloon angioplasty and in neo-intimal cells at 7 and 14 days. Smad3 was also expressed in neo-intimal cells at 7 and 14 days post-angioplasty suggesting that TGFβ, through Smad3, is responsible for Wnt/β-Catenin activation during vascular injury. In conclusion, this work describes a novel cross-talk in SMCs between TGFβ and Wnt signaling which may provide a viable target for future anti-restenotic treatments.

scholarly journals Hormone Replacement Therapy Influences Matrix Metalloproteinase Expression and Intimal Hyperplasia Development after Vascular Injury: A Follow-Up Study

2010 ◽  
Vol 52 (6) ◽  
pp. 1744
Author(s):  
Richard B. Cook ◽  
Deidra J. Mountain ◽  
Stacy S. Kirkpatrick ◽  
James E. Chalk ◽  
David C. Cassada ◽  
...  
Keyword(s):  
Hormone Replacement Therapy ◽  
Matrix Metalloproteinase ◽  
Replacement Therapy ◽  
Vascular Injury ◽  
Intimal Hyperplasia ◽  
Hormone Replacement ◽  
Follow Up Study

scholarly journals Aralia armata (Wall.) Seem Improves Intimal Hyperplasia after Vascular Injury by Downregulating the Wnt3α/Dvl-1/β-Catenin Pathway

2021 ◽  
Vol 2021 ◽  
pp. 1-12
Author(s):  
Xiangpei Zhao ◽  
Jinchang Huang ◽  
Zhenyu Mo ◽  
Jiangcun Wei ◽  
Chuanmei Zhong ◽  
...  
Keyword(s):  
Vascular Injury ◽  
Femoral Artery ◽  
Intimal Hyperplasia ◽  
Dose Group ◽  
High Dose ◽  
Sham Operation ◽  
Model Group ◽  
And Migration ◽  
Gsk 3Β ◽  
Proliferation And Migration

The aim of the study is to examine the mechanism of Aralia armata (Wall.) Seem (AAS) in improving intimal hyperplasia after vascular injury in rats. Rats with femoral artery injury were randomly divided into three groups: the model group, AAS low-dose group (40 mg/kg), and AAS high-dose group (80 mg/kg). The sham operation group was used as a control group. HE staining was used to observe the changes in femoral artery vessels. Immunohistochemistry was adopted to detect α-SMA, PCNA, GSK-3β, and β-catenin proteins in femoral artery tissue. The CCK-8 test and wound healing assay were employed to analyze the effect of AAS on proliferation and migration of vascular smooth muscle cells (VSMCs) cultured in vitro. Western blotting (WB) and polymerase chain reaction (PCR) assays were used to evaluate the molecular mechanism. AAS reduced the stenosis of blood vessels and the protein expressions of α-SMA, PCNA, GSK-3β, and β-catenin compared to the model group. In addition, AAS (0-15 μg/mL) effectively inhibited the proliferation and migration of VSMCs. Moreover, the results of WB and PCR showed that AAS could inhibit the activation of β-catenin induced by 15% FBS and significantly decrease the expression levels of Wnt3α, Dvl-1, GSK-3β, β-catenin, and cyclin D1 in the upstream and downstream of the pathway. AAS could effectively inhibit the proliferation and migration of neointima after vascular injury in rats by regulating the Wnt/β-catenin signaling pathway.

scholarly journals Intimal hyperplasia after vascular injury is inhibited by antisense cdk 2 kinase oligonucleotides.

1994 ◽  
Vol 93 (4) ◽  
pp. 1458-1464 ◽  
Author(s):  
R Morishita ◽  
G H Gibbons ◽  
K E Ellison ◽  
M Nakajima ◽  
H von der Leyen ◽  
...  
Keyword(s):  
Vascular Injury ◽  
Intimal Hyperplasia
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