scholarly journals Intimal Hyperplasia in Loop-Injured Carotid Arteries Is Attenuated in Transglutaminase 2-Null Mice

2014 ◽  
Vol 29 (3) ◽  
pp. 363 ◽  
Author(s):  
Seung-Kee Min ◽  
Sang-Il Min ◽  
Eui Man Jeong ◽  
Sung-Yup Cho ◽  
Jongwon Ha ◽  
...  
2004 ◽  
Vol 24 (11) ◽  
pp. 2063-2068 ◽  
Author(s):  
Ryo Gotoh ◽  
Jun-ichi Suzuki ◽  
Hisanori Kosuge ◽  
Tsunekazu Kakuta ◽  
Shinji Sakamoto ◽  
...  

EBioMedicine ◽  
2015 ◽  
Vol 2 (11) ◽  
pp. 1650-1661 ◽  
Author(s):  
Bowen Wang ◽  
Mengxue Zhang ◽  
Toshio Takayama ◽  
Xudong Shi ◽  
Drew Alan Roenneburg ◽  
...  

2001 ◽  
Vol 7 (1_suppl) ◽  
pp. 161-166 ◽  
Author(s):  
S. Nishi ◽  
Y. Nakayama ◽  
H. Ueda ◽  
M. Ishikawa ◽  
T. Matsuda

The use of stents has improved results after balloon carotid angioplasty. Some materials have been reported for covering the metal surface of the stent to reduce the rate of subacute thrombosis and restenosis. We have already developed a new stent graft with thin-walled controlled micropored polymer covering, and in a previous study we confirmed tissue ingrowth via the micropores at one month in a beagle model. The progress of cell migration was controlled by micropore density using a constant micropore diameter (30μm diameter, 125μm inter-pore distance). In the present study, we applied our newly developed stent graft impregnated with heparin for implantation in the rabbit carotid artery, and carried out an angiographic and histological investigation. Our stent graft was made from a Palmaz-Schatz stent and a micropored segmental polyurethane (SPU) thin film with a heparin coating. Micropores 30μm in diameter and 125μm apart were created on the thin SPU film using an excimer laser ablation technique. The surface of the micropored film was then impregnated with photosensitive gelatin that incorporated the heparin. The metal stent was rolled up and fixed to this modified SPU film under microscopic observations. These stent grafts were deployed in the common carotid arteries (CCAs) of rabbits (37 carotid arteries, 20 rabbits). The animals were sacrificed one, two and three months later, and a histological study and scanning electron microscopy study were performed for evaluation of endoluminal endothe-lialization and intimal thickening at the late stage. CCAs treated with stent grafts of micropored film showed poor-patency and intimal hyperplasia compared with those treated with a simple bare stent or a heparin-impregnated stent. In terms of intimal hyperplasia and patency, the heparin-impregnated stent was superior to the bare stent. Intimal hyperplasia was prevented by control of tissue ingrowth through the micropores. The antithrombogenicity of the impregnated heparin improved patency in the early stage. Our new stent graft with a heparin-impregnated SPU film thus appears promising for prevention of restenosis due to neointimal hyperplasia.


2001 ◽  
Vol 12 (1) ◽  
pp. 79-88 ◽  
Author(s):  
Pierre E. Signore ◽  
Lindsay S. Machan ◽  
John K. Jackson ◽  
Helen Burt ◽  
Peter Bromley ◽  
...  

2014 ◽  
Vol 2014 ◽  
pp. 1-5
Author(s):  
Julius Ogeng’o ◽  
Kevin Ongeti ◽  
Moses Obimbo ◽  
Beda Olabu ◽  
Philip Mwachaka

Introduction. Histologic changes which occur in the tunica adventitia during initiation, progression, and complications of atherosclerosis are seldom reported. This study aimed at describing the features of atherosclerosis in the tunica adventitia of two of the commonly afflicted arteries, namely, left anterior descending coronary and common carotid in black Kenyans. Materials and Methods. Specimens from 108 individuals [76 males and 32 females, mean age 34.6] were processed for paraffin embedding. Seven micron thick sections were stained with Mason’s trichrome and Haematoxylin/Eosin and examined with a light microscope. Results. Features of atherosclerosis were present in the tunica adventitia of 14.8% of left anterior descending arteries and 11.1% of common carotid arteries. Increase in adventitial thickness was associated with increased density of vasa vasora in 8.3% of both arteries. In the left anterior descending and common carotid arteries, 6.5% and 3.7% of cases, respectively, the tunica adventitia thickened without intimal hyperplasia. Conclusion. Features of atherosclerosis occur in the tunica adventitia of coronary and carotid arteries in over 10% of the black Kenyans studied. These features often precede the intimo medial changes. Tunica adventitia should therefore be prioritized in evaluation for atherosclerosis, in individuals at risk. This may enhance early detection and intervention.


Circulation ◽  
2001 ◽  
Vol 103 (10) ◽  
pp. 1446-1452 ◽  
Author(s):  
Jia-Li Gu ◽  
Hong Pei ◽  
Lisa Thomas ◽  
Jerry L. Nadler ◽  
John J. Rossi ◽  
...  

2006 ◽  
Vol 39 (1) ◽  
pp. 54-54
Author(s):  
Takeshi Wakamatsu ◽  
Takashi Saito ◽  
Junichi Hayashi ◽  
Toshiaki Takeichi ◽  
Kiyoshi Kitamoto ◽  
...  

2021 ◽  
Vol 10 (22) ◽  
pp. 5449
Author(s):  
Genhuan Yang ◽  
Rong Zeng ◽  
Xitao Song ◽  
Changwei Liu ◽  
Leng Ni

Introduction: Balloon angioplasty is a commonly applied procedure for treating atherosclerotic vascular diseases. However, the maintenance of long-term lumen patency is relatively difficult due to the occurrence of restenosis. Previous research has shown that the occurrence of vascular wall inflammation is associated with higher rates of restenosis. Sophocarpine (SPC) can exert various therapeutic effects such as anti-oxidation, anti-inflammation, anti-tumor, antivirus and immune regulation. This study aimed to investigate whether SPC can alleviate intimal hyperplasia following balloon injury in a rat carotid artery model. Methods: Twenty Sprague–Dawley rats were randomly assigned to four groups: (i) control, (ii) balloon injury, (iii) balloon injury followed by saline injection, and (iv) balloon injury followed by SPC administration. Each group contained five rats. A high-pressure balloon of 3 mm × 20 mm was placed in the carotid artery. The balloon was inflated to a pressure of 8 atmospheres to carry out rat carotid artery balloon injury model. The areas of neointimal and media were determined by Verhoeff_Van Gieson staining, and the intima-to-media (I:M) ratios were subsequently evaluated. After that, the protein levels of IL-6, IL-1β, MCP-1, NF-κB, TNF-α, VCAM-1, ICAM-1 and eNOS were measured. Results: The ratio of I:M was remarkably higher in the balloon injury group than in the control group (p < 0.01). SPC could significantly decrease the ratio of I:M compared with the balloon injury group (p < 0.01). Besides, the protein levels of IL-6, IL-1β, MCP-1, NF-κB, TNF-α, ICAM-1 and VCAM-1 were increased in rat carotid arteries exposed to balloon injury (p < 0.01), and treatment with SPC could attenuate these effects (p < 0.05). Furthermore, balloon injury inhibited the protein expression of eNOS (p < 0.01), and SPC could elevate its level (p < 0.05). Conclusions: SPC could alleviate an intimal hyperplasia in balloon-injured carotid artery, and the mechanisms underlying this protective effect might be due to its inhibitory potency against inflammation signals. Our study also implies the potential applicability of SPC in treating restenosis after balloon angioplasty.


Author(s):  
Yung-Chun Wang ◽  
Dunpeng Cai ◽  
Xiao-Bing Cui ◽  
Ya-Hui Chuang ◽  
William P. Fay ◽  
...  

Objective: The objective of this study is to determine the role of JAK3 (Janus kinase 3) in reendothelialization after vascular injury. Methods and Results: By using mouse carotid artery wire injury and rat balloon injury model, we found that JAK3 regulates reendothelialization and endothelial cell proliferation after vascular injury. JAK3 and phospho-JAK3 levels were increased in neointimal smooth muscle cells in response to vascular injury in mice. JAK3 deficiency dramatically attenuated the injury-induced intimal hyperplasia in carotid arteries of both male and female mice. Importantly, JAK3 deficiency caused an increased rate of reendothelialization following mechanical injury. Likewise, knockdown of JAK3 in medial smooth muscle cells elicited an accelerated reendothelialization with reduced intimal hyperplasia following balloon injury in rat carotid arteries. Interestingly, knockdown of JAK3 restored the expression of smooth muscle cell contractile protein smooth muscle α-actin in injury-induced intimal smooth muscle cells while increased the proliferating endothelial cells in the intima area. Conclusions: Our results demonstrate a novel role of JAK3 in the regeneration of endothelium after vascular injury, which may provide a new strategy to enhance reendothelialization while suppressing neointimal formation for effective vascular repair from injury.


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