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首页> 外文期刊>Cardiology >Increased Mobilization of CD45+CD34+VLA-4+Cells in Acute Viral Myocarditis Induced by Coxsackievirus B3
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Increased Mobilization of CD45+CD34+VLA-4+Cells in Acute Viral Myocarditis Induced by Coxsackievirus B3

机译:Coxsackievirus B3诱导的急性病毒心肌炎中CD45 + CD34 + VLA-4 +细胞的调节增加

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Objectives: Bone marrow-derived cells (BMCs) have recently been identified to play a vital role in repairing damaged myocardium; however, it is not known whether or not mobilization of BMCs is involved in the pathogenesis of acute viral myocarditis (VMC). Thus, we analyzed the expression of CD45+CD34+VLA-4+ cells and vascular cell adhesion protein-1 (VCAM-1) in a murine model of acute VMC. Methods: Male BALB/c mice were intraperitoneally infected with coxsackievirus B3 to establish acute VMC. The frequency of CD45+CD34+VLA-4+ cells in the heart, peripheral blood, and bone marrow was examined by flow cytometry 3, 7, 14, and 28 days after injection. Cardiac VCAM-1 and pathology scores were determined by immunohistochemistry, and myocardial VCAM-1, IL-1 beta, and TNF-alpha were analyzed by RTPCR and Western blot. Results: In mice with acute VMC, the CD45+CD34+VLA-4+ cell population in the heart was significantly increased by day 7 and then decreased; in contrast, the CD45+CD34+VLA-4+ cell population decreased in the bone marrow and peripheral blood by day 3 and then increased. High expression of VCAM-1 was detected in the heart in parallel with CD45+CD34+VLA-4+ cell expression. Conclusions: In mice with acute VMC, VCAM-1-induced CD45+CD34+VLA-4+ cell mobilization into the injured heart is involved in the repair of injured myocardium. (c) 2017 S. Karger AG, Basel
机译:目的:最近已识别骨髓衍生的细胞(BMC)在修复受损心肌中起着至关重要的作用;然而,不知道BMC的动员是否参与急性病毒性心肌炎的发病机制(VMC)。因此,我们在急性VMC的鼠模型中分析了CD45 + CD34 + VLA-4 +细胞和血管细胞粘附蛋白-1(VCAM-1)的表达。方法:雄性BALB / C小鼠腹膜内感染COXSackeivirus B3以建立急性VMC。通过喷射后的流式细胞术3,7,14和28天检查心脏,外周血和骨髓中CD45 + CD34 + VLA-4 +细胞的频率。通过免疫组织化学确定心脏VCAM-1和病理学分数,并通过RTPCR和Western印迹分析心肌VCAM-1,IL-1β和TNF-α。结果:在急性VMC的小鼠中,第7天,心脏中CD45 + CD34 + VLA-4 +细胞群明显增加,然后减少;相反,CD45 + CD34 + VLA-4 +细胞群在骨髓和外周血中减少了第3天,然后增加。与CD45 + CD34 + VLA-4 +细胞表达平行地在心脏中检测VCAM-1的高表达。结论:在急性VMC的小鼠中,VCAM-1诱导的CD45 + CD34 + VLA-4 +细胞动员进入受伤心脏的伤害心肌。 (c)2017年S. Karger AG,巴塞尔

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