Matrix metalloproteinase (MMP)-3 activates MMP-9 mediated vascular smooth muscle cell migration and neointima formation in mice. (73/339)

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In vivo virtual histology intravascular ultrasound comparison of neointimal hyperplasia within drug-eluting- versus bare metal stents. (74/339)

BACKGROUND: The process of in-stent neointimal hyperplasia (NIH) between drug-eluting stents (DES) and bare metal stents (BMS) might be different. We compared in vivo composition of in-stent NIH between DES and BMS using virtual histology-intravascular ultrasound (VH-IVUS). METHODS AND RESULTS: Volumetric VH-IVUS was used to compare in-stent NIH between 23 DES and 15 BMS in 30 patients who underwent coronary angiography because of angina. The inner and outer VH-IVUS contours were drawn in a way to avoid the stent strut artifacts. Cross-sectional analysis was done at every VH-IVUS frame within the stent, thereby allowing volumetric measurement of stent, lumen, and NIH and its components. Baseline characteristics and IVUS measurements were similar between DES and BMS groups. The duration of follow-up was similar between DES (median 38 months [interquartile range, 7-59]) vs. BMS (median 40 months [interquartile range, 7-99]), (p=0.26). % necrotic core (NC) volume was significantly higher in DES than BMS: 19.5 [16.3, 25.6] vs. 12.1 [8.2, 18.5] (p=0.006). %NC volume significantly increased with time in BMS (p=0.007), but not in DES (p=0.24) so that at any given time point, %NC in DES was greater than in BMS. After adjustment for baseline differences, only DES (p=0.003) and stent age (p=0.043) were independent predictors of %NC volume. VH-IVUS in-stent thin-cap fibroatheromas were detected only in the DES group: 34.8% vs. 0%, p=0.013. CONCLUSION: In vivo composition of in-stent NIH between DES and BMS was different, suggesting that the process of in-stent NIH in DES and BMS is diverse.  (+info)

Late lumen loss and intima hyperplasia after sirolimus-eluting and zotarolimus-eluting stent implantation in diabetic patients: the diabetes and drug-eluting stent (DiabeDES III) angiography and intravascular ultrasound trial. (75/339)

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Paclitaxel-iopromide coated balloon followed by "bail-out" bare metal stent in porcine iliofemoral arteries: first report on biological effects in peripheral circulation. (76/339)

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Orai1-mediated I (CRAC) is essential for neointima formation after vascular injury. (77/339)

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Effect of adiponectin on cardiac allograft vasculopathy. (78/339)

BACKGROUND: The role of adiponectin (APN), an adipose tissue-specific secretory protein, on chronic rejection after cardiac transplantation in APN-sense transgenic mice (APN-SE) was evaluated. METHODS AND RESULTS: Heterotopic cardiac transplantation in major histocompatibility complex class II-mismatched mice was performed. B6.C-H-2(bm12)KhEg (Bm12) hearts were transplanted into APN-SE, and allografts were harvested at 8 weeks after transplantation. Quantitative polymerase chain reaction (PCR) and immunohistochemical staining showed that the expression of both AdipoR1 and AdipoR2 was induced in APN-SE recipients. Neointimal hyperplasia was significantly decreased in allografts transplanted into APN-SE (luminal occlusion, 8.9 +/- 2.2%) compared to those transplanted into controls (49.4 +/- 10.5%; P=0.011). APN-SE showed significantly reduced mRNA levels of interferon (IFN)-gamma, tumor necrosis factor (TNF)-alpha, interleukin (IL)-2, IL-6, and monocyte chemoattractant protein-1 (MCP-1) by quantitative PCR. Western blot analysis revealed that the protein levels of IFN-gamma and MCP-1 were reduced in APN-SE recipients. Proliferation of smooth muscle cells stimulated with activated T cells was suppressed by APN addition, and this effect was canceled by treatment with an adenosine monophosphate-activated protein kinase (AMPK) inhibitor. CONCLUSIONS: APN plays a critical role in the attenuation of chronic rejection by suppressing inflammatory cytokine and chemokine expression and enhancing APN receptor expression. APN plays a beneficial role in reducing the progression of cardiac allograft vasculopathy through the AMPK pathway.  (+info)

Neutrophil elastase is produced by pulmonary artery smooth muscle cells and is linked to neointimal lesions. (79/339)

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Increased plasma chymase concentration and mast cell chymase expression in venous neointimal lesions of patients with CKD and ESRD. (80/339)

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