Human mesenchymal stromal cells (MSCs) reduce neointimal hyperplasia in a mouse model of flow-restriction by transient suppression of anti-inflammatory cytokines.
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AIM: Mesenchymal stromal cells from human bone marrow (hMSCs) were observed to produce therapeutic benefits in some models for cardiac and vascular injuries but their mode of action was not defined. We tested the effects of hMSCs in models for restricted vascular flow. METHODS: We made model for restricted vascular flow produced by permanent ligation of a carotid artery and injected hMSCs to clarify the effects of hMSCs to vascular lesions. RESULTS: Seven, 14, and 28 days after infusion of hMSCs into the cardiac left ventricle of the mice, there was a significant reduction in neointimal hyperplasia (p<0.05). Seven days after administration of the hMSCs, macrophages infiltration into the ligated artery and serum levels of monocyte chemoattractive protein-1 (MCP-1/CCL-2) (p<0.05) were reduced. However, no hMSCs were detected in the lesions by sensitive PCR assays. We then observed that the serum level of MCP-1 was a potential biomarker for the therapeutic effects of hMSCs in a mouse model for high-fat-diet. CONCLUSIONS: These results indicated the administration of hMSCs decreased the initial and excess inflammatory responses to carotid artery ligation. The decrease in inflammatory response apparently decreased the subsequent neointimal hyperplasia. (+info)
Qualitative assessment of neointimal tissue after drug-eluting stent implantation: comparison between follow-up optical coherence tomography and intravascular ultrasound.
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Possible role of damaged neoendothelial cells in the genesis of coronary stent thrombus in chronic phase. A dye staining angioscopic study.
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The mechanism(s) underlying formation of coronary stent thrombus (ST) in chronic phase is yet unclear. Endothelial cells are highly antithrombotic, therefore, it is conceivable that neoendothelial cells (NECs) covering stent struts are damaged and cause ST. This study was performed to examine the role of damaged NECs covering coronary stent struts in the genesis of occlusive or nonocclusive ST in chronic phase.(1) Forty-four patients with acute coronary syndrome (17 females and 27 males) underwent dye-staining coronary angioscopy, using Evans blue which selectively stains damaged endothelial cells, 6 months after bare-metal stent (BMS) deployment. Neointimal coverage was classified into not covered (grade 0), covered by a thin layer (grade 1), and buried under neointima (grade 2) groups. (2) In 7 beagles, the relationships between neointimal thickness and ST were examined 6 months after BMS deployment. (3) The NECs on the struts were stained blue in 4 of 25 patients with grade 2 and in 11 of 20 patients with grade 0/1 (P < 0.05). ST was observed in none of the former and in 5 of the latter (P < 0.05). (4) In beagles, neointimal coverage was grade 0/1 when neointimal thickness was 80.2 +/- 40.0 microm, whereas grade 2 when thickness was 184 +/- 59.4 microm. ST was observed in 9 of 15 struts with neointimal thickness within 100 microm and in one of 17 struts with thickness over 100 microm (P < 0.05). ST arose from damaged NECs covering the stent struts. NECs may have been damaged due to friction between them and struts due to thin interposed neointima which might have acted as a cushion, resulting in ST. (+info)
Comparison of diamond-like carbon-coated nitinol stents with or without polyethylene glycol grafting and uncoated nitinol stents in a canine iliac artery model.
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The relationship between carotid intima media thickness and oxidative stress in asthmatic children.
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BACKGROUND: Asthma and atherosclerosis are both chronic inflammatory diseases. The progression of the inflammation in asthmatic patients is known to be similar to the increased development of atherosclerosis. OBJECTIVE: The aim of this study was to research the relationship between the difference in carotid intima media thickness (CIMT) and oxidative stress together with difference in CIMT in asthmatic children and control group. METHODS: A total of 84 subjects between 6-15 years of age who had been attending the Pediatric Allergy Unit of the Medical Faculty were included in this study. Asthmatic patients and a control group were evaluated by ultrasonography for measurements of CIMT and oxidative status. RESULTS: In the asthmatic patient group, the CIMT was 0.48 +/- 0.06 mm (right side) and 0.44 +/- 0.05 mm (left side). In the control group it was 0.42 +/- 0.05 mm (right side) and 0.42 +/- 0.04 mm (left side). This difference is statistically significant (p < 0.0001, p = 0.019 respectively). In the asthmatic group a positive correlation was determined between the total oxidant status (TOS) value and the right and left CIMT (p = 0.007, r = 0.44 and p = 0.001, r = 0.50 respectively). CONCLUSIONS: A significant correlation was determined between an increase in oxidative stress and CIMT in asthmatic children. This indicates that atherosclerosis, which is known as an adult disease, may start in childhood. These findings show that it might be beneficial for children who are being followed-up from a diagnosis of asthma to also be evaluated in respect of the development of atherosclerosis. (+info)
Poly(diol-co-citrate)s as novel elastomeric perivascular wraps for the reduction of neointimal hyperplasia.
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Protein tyrosine phosphatase SHP-2 is positively involved in platelet-derived growth factor-signaling in vascular neointima formation via the reactive oxygen species-related pathway.
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The roles of Src homology domain 2-containing protein tyrosine phosphatase 2 (SHP-2) and its signaling in atherosclerosis have not been explored. Therefore, we investigated the roles of SHP-2 in the movement of rat aortic smooth muscle cells (RASMCs) and in the neointima formation of the carotid artery. Platelet-derived growth factor (PDGF)-BB (1 - 20 ng/ml) increased the activity and phosphorylation of SHP-2 and migration in RASMCs and these were suppressed by SHP-2 inhibitor NSC-87877 (30 microM) and small interfering RNA of SHP-2. PDGF-BB increased the phosphorylations of spleen tyrosine kinase (Syk) and p38 mitogen-activated protein kinase (MAPK), which were recovered by inhibition of SHP-2. Moreover, PDGF-BB increased the levels of reactive oxygen species (ROS) and ROS inhibitors decreased PDGF-BB-increased migration. Treatment of RASMCs with H(2)O(2) (100 microM) increased cell migration and SHP-2 phosphorylation and also enhanced the phosphorylation levels of Syk and p38 MAPK. Oral administration of NSC-87877 (10 mg/kg) significantly suppressed neointima formation in a rat model of carotid artery injury. These results suggest that the activity of SHP-2 is controlled by ROS and is positively involved in the regulation of PDGF-BB-induced RASMC migration and neointima formation. (+info)