scholarly journals Succinobucol‐eluting stents increase neointimal thickening and peri‐strut inflammation in a porcine coronary model

2012 ◽  
Vol 81 (4) ◽  
pp. 698-708 ◽  
Author(s):  
Jonathan Watt ◽  
Simon Kennedy ◽  
Christopher McCormick ◽  
Ejaife O. Agbani ◽  
Allan McPhaden ◽  
...  
Keyword(s):  
Neointimal Thickening

Influence of External Stent Size on Early Medial and Neointimal Thickening in a Pig Model of Saphenous Vein Bypass Grafting

Circulation ◽  
1996 ◽  
Vol 94 (7) ◽  
pp. 1741-1745 ◽  
Author(s):  
Mohammad Bashar Izzat ◽  
Dheeraj Mehta ◽  
Alan J. Bryan ◽  
Barnaby Reeves ◽  
Andrew C. Newby ◽  
...  
Keyword(s):  
Saphenous Vein ◽  
Pig Model ◽  
Bypass Grafting ◽  
Neointimal Thickening ◽  
Saphenous Vein Bypass ◽  
Vein Bypass

Hemodynamically “insignificant” stenoses stimulate neointimal thickening in experimental vein grafts

2011 ◽  
Vol 10 (02) ◽  
pp. 92-95
Author(s):  
Shari Meyerson ◽  
Daniel Refai ◽  
Christopher Skelly ◽  
Michael Curi ◽  
Seymour Glagov ◽  
...  
Keyword(s):  
Vein Grafts ◽  
Neointimal Thickening

scholarly journals Aged Rats Have Increased Neointimal Thickening and Ephrin-B2 Expression After Carotid Angioplasty

2010 ◽  
Vol 52 (3) ◽  
pp. 817
Author(s):  
Sammy D.D. Eghbalieh ◽  
Jose M. Pimiento ◽  
Fabio A. Kudo ◽  
Akihito Muto ◽  
Kenneth R. Ziegler ◽  
...  
Keyword(s):  
Carotid Angioplasty ◽  
Aged Rats ◽  
Neointimal Thickening

Neointimal thickening resulting in artery stenosis following renal sympathetic denervation

2014 ◽  
Vol 177 (3) ◽  
pp. e117-e119 ◽  
Author(s):  
Mihaela-Elena Cordeanu ◽  
Sébastien Gaertner ◽  
François Bronner ◽  
Christine Jahn ◽  
Eric Prinz ◽  
...  
Keyword(s):  
Artery Stenosis ◽  
Sympathetic Denervation ◽  
Renal Sympathetic Denervation ◽  
Neointimal Thickening ◽  
Renal Sympathetic

Aged Rats Have Increased Neointimal Thickening And Altered MCP-1/CCR2 Expression After Carotid Angioplasty

2011 ◽  
Vol 165 (2) ◽  
pp. 184
Author(s):  
S.D. Eghbalieh ◽  
P. Chowdhary ◽  
J.M. Pimiento ◽  
F.A. Kudo ◽  
K.R. Ziegler ◽  
...  
Keyword(s):  
Carotid Angioplasty ◽  
Aged Rats ◽  
Neointimal Thickening ◽  
Ccr2 Expression

Abstract 5494: ADAMTS-7 is Critical for Vascular Smooth Muscle Cell Migration and Neointima Formation in Injured Rat Carotid Artery

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Wei Kong ◽  
Li Wang ◽  
Xue Bai ◽  
Bo Liu ◽  
Yi Zhu ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Vascular Injury ◽  
Matrix Protein ◽  
Mrna Level ◽  
Balloon Catheter ◽  
Migration And Invasion ◽  
Neointima Formation ◽  
Subsequent Increase ◽  
Neointimal Thickening

Migration of vascular smooth muscle cells (VSMCs) plays an essential role during vascular development, in response to vascular injury and during atherogenesis. Extensive studies have implicated the importance of extracellular matrix (ECM)-degrading proteinases during VSMCs migration. ADAMTS (a disintegrin and metalloproteinase with thrombospondin motifs), a recently described family of proteinases, is capable of degrading vascular ECM proteins. However, the relevance of ADAMTS family members in cardiovascular disease is poorly understood. In this study, we sought to determine whether ADAMTS-7 is involved in VSMC migration and neointima formation in response to vascular injury. Denudation of rat carotid arteries with a balloon catheter led to an initial decrease of ADAMTS-7 protein level in injured compared with sham-operated arteries within the first 24 hours, followed by a subsequent increase during the 4 to 14 days after injury. In primary VSMCs, the pro-inflammatory cytokine TNF-α increased ADAMTS-7 mRNA level through transcriptional factors nuclear factor-kappa B and AP-1. VSMCs infected with ADAMTS-7 adenovirus (Ad-ADAMTS-7) greatly accelerated their migration and invasion in vitro . Conversely, suppression of ADAMTS-7 expression by small interfering RNA (siRNA) markedly retarded VSMC movement by 50% than that with scramble siRNA. At 7 days after injury, the neointimal area of the vascular wall was sixfold greater in Ad-ADAMTS-7-infected than that in Ad-GFP-infected vessels (3.10±0.88 vs. 0.52±0.28 ×10 4 μm 2 , n=8 per group, P <0.05). By contrast, perivascular administration of ADAMTS-7 siRNA, but not scramble siRNA to injured arteries resulted in prolonged ADAMTS-7 silencing and diminished neointimal thickening without affecting medial areas. This inhibitory effect was sustained up to 14 days after injury. As well, ADAMTS-7 mediated degradation of the vascular ECM cartilage oligomeric matrix protein (COMP) in injured vessels, which might facilitate VSMC migration and neointimal thickening. ADAMTS-7 directs VSMC migration and neointima formation and therefore may serve as a novel therapeutic target for vascular restenosis and atherogenesis.

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