首页> 外文会议>Nordrhein-Westfa?lische Akademie der Wissenschaften >Blockade of keratinocyte-derived chemokine inhibits endothelial recovery and enhances plaque formation after arterial injury in apolipo-protein E-deficient mice
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Blockade of keratinocyte-derived chemokine inhibits endothelial recovery and enhances plaque formation after arterial injury in apolipo-protein E-deficient mice

机译:表达角质形成细胞衍生的趋化因子抑制内皮恢复,并增强脂蛋白缺乏小鼠动脉损伤后的斑块形成

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We evaluated the involvement of keratinocyte-derived chemokine (KC) in neointimal hyperplasia and endothelial repair following arterial injury.Wire-induced injury of common carotid arteries in apolipoprotein E-deficient (apoE_/") mice treated with either a neutralizing monoclonal anti-KC or isotype control antibody (twice weekly, 50 ug per injection, n=6 per group) for three weeks on high cholesterol diet was performed. Serial sections of the carotid artery were stained with Movats pentachrome and analyzed for arterial wall. a-SMA, Mac-2 plaque content and CD31 and VE-Cadherin positive luminal cells were determined. Carotid sections were co-stained for KC or CXCR2 and cell-specific markers (Mac-2 or CD31).
机译:在动脉损伤后,通过中和单克隆抗KC治疗的载脂蛋白E缺陷(APOE_ /“)小鼠常见的颈动脉均致颈动脉造成的肺癌常见动脉损伤,评估了角质形成细胞衍生的趋化因子(KC)。在高胆固醇饮食中进行三次对照抗体(每周两次,每次注射,每组N = 6)三周。颈动脉的连续部分用Movats Pentachrome染色并分析动脉壁。A-SMA,测定MAC-2斑块含量和CD31和VE-CADHERIN正腔细胞。颈动脉切片被共染成KC或CXCR2和细胞特异性标记物(MAC-2或CD31)。

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