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作 者:刘明[1] 许心舒[2] 乔东访[3] 汪冠三[2] 郑丽霞[1] 王慧君[3]
机构地区:[1]广州医学院第一附属医院呼吸疾病研究所,呼吸疾病国家重点实验室,广东广州510120 [2]广州市公安局刑事科学技术研究所,广东广州510030 [3]南方医科大学法医学研究所,广东广州510515
出 处:《南京医科大学学报(自然科学版)》2013年第5期604-609,共6页Journal of Nanjing Medical University(Natural Sciences)
基 金:国家自然科学基金(30370588,81200050);呼吸疾病国家重点实验室青年项目(2011-A8)
摘 要:目的:调查心肌肌球蛋白轻链4(myosin light polypeptide 4,MYL4)在病毒性心肌炎损伤中的作用。方法 :随机将Balb/c小鼠分为实验组(n=30)和对照组(n=10),实验组用于建立柯萨奇病毒B3病毒性心肌炎小鼠模型,分别在病毒感染后第3、7、14天留取心脏及血清标本。利用差异蛋白质组学的方法鉴定了部分的病毒性心肌炎差异表达蛋白,并对其中一个分子MYL4在病毒性心肌炎发病中的作用进行研究。结果:质谱鉴定6个差异表达分子分别为:MYL4、热休克蛋白B1、异柠檬酸脱氢酶a亚单位、电压依赖的阴离子通道蛋白、蛋白酶体a亚单位1型和巨噬细胞封端蛋白。Western blot及ELISA验证发现MYL4在病毒性心肌炎小鼠心脏组织及血清中表达明显升高(P<0.01),且ELISA结果显示MYL4的表达与疾病严重程度呈正相关(r=0.97,P<0.00)。结论:MYL4在病毒性心肌炎组织及血清中表达升高,参与了病毒性心肌炎的发生发展。Objective:To investigate the effects and mechanism of myosin light polypeptide 4 (MYIA) on injury caused by viral myocarditis in mice. Methods:The experimental animals were randomly divided into the viral myoearditis group (n = 30) and the control group (u = 10). The viral myocarditis models were achieved by infection with coxsackievirus B3 (CVB3). The proteomics assay was performed to identify the different proteins involve in the pathogenesis of viral myocarditis. The expression and the role of one identified protein MYL4 were evaluated by Western Hot and ELISA. Results: Six proteins were successfully identified by MS: MYL4, heat shock protein β1, isocitrate dehydrogenase subunit α mitochondrial precursor, voltage dependent anion-selective channel protein 2, proteasome subunit c~ type 1 and macrophage capping protein. The expression of MYL4 was higher in the heart tissue and serum of VMC mice (P 〈 0.01), and ELISA results showed that the expression of MYIA was related to the severity of disease (r = 0.97,P 〈 0.00). Conclusion:The MYIA expression of VMC was higher than that of the control group, and also could indicate the injury degree, which suggesting that MYIA might be involved in the pathogenesis of VMC.
关 键 词:柯萨奇病毒B3 心肌炎 蛋白质组学 肌球蛋白轻链4
分 类 号:R542.21[医药卫生—心血管疾病]
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