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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:骨髓源性细胞(BMC)在修复受损心肌中起着重要作用;然而,目前尚不清楚BMC动员是否参与急性病毒性心肌炎(VMC)的发病机制。因此,我们分析了急性VMC小鼠模型中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小鼠腹腔感染柯萨奇B3病毒,建立急性VMC模型。注射后3、7、14和28天,通过流式细胞术检测心脏、外周血和骨髓中CD45+CD34+VLA-4+细胞的频率。通过免疫组织化学测定心肌VCAM-1和病理学评分,并通过RTPCR和Western blot分析心肌VCAM-1、IL-1β和TNFα。结果:在急性VMC小鼠中,心脏中的CD45+CD34+VLA-4+细胞群在第7天显著增加,然后下降;相反,在第3天,骨髓和外周血中的CD45+CD34+VLA-4+细胞群减少,然后增加。在心脏中检测到VCAM-1的高表达与CD45+CD34+VLA-4+细胞表达平行。结论:在急性VMC小鼠中,VCAM-1诱导的CD45+CD34+VLA-4+细胞进入受损心脏参与了受损心肌的修复。(c) 2017年巴塞尔S.卡格股份公司

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