心肌肥大是心血管疾病重要的病理过程,涉及能量代谢紊乱、收缩功能失调和细胞凋亡等多种病理生理机制,蛋白质作为生命活动的执行体,参与了上述多种病理过程,导致心肌肥大的发生、发展。本实验旨在采用双向电泳(2-D electrophoresis,2-DE)和质谱分析技术探讨腹主动脉狭窄诱导大鼠心肌肥大后心肌组织蛋白质表达谱的变化。健康雄性Wistar大鼠12只随机分为模型组和对照组(n=6),模型组行腹主动脉缩窄术,对照组仅分离腹主动脉不行缩窄术,术后4周结束实验并提取左心室组织蛋白质,双向电泳技术分离心肌组织蛋白质,考马斯亮兰R-250染色后,计算机图像分析差异显示的蛋白质并选取9个差异显著的蛋白点进行胶内酶切和质谱分析(matrix-assisted laser desorption/ionization-time of flight mass spectrometry,MALDI- TOF)。结果发现双向电泳可分离454±13个蛋白质,点匹配率为(78.7±1.4)%,心肌组织13种蛋白质出现明显差异表达,其中4种蛋白质表达在模型组上调,9种蛋白质表达在模型组下调。质谱分析鉴定出7个蛋白质为:与能量代谢相关的丙酮酸脱氢酶E1(pyruvate dehydrogenase E1,PDH)和β-烯醇酶(β-enolase),与细胞收缩功能相关的α-肌球蛋白重链(α-myosin heavy chain,α-MHC)、肌球蛋白轻链(myosin light chain,MLC)和心脏α-肌动蛋白前体(α-actin proprotein),与细胞内源性保护相关的热休克蛋白B6(heat shock protein B6,HspB6),以及与甲状腺激素代谢相关的甲状腺素结合蛋白(transthyretin,TTR)等几组蛋白质。其中PDH、β-烯醇酶、α-MHC、α-actin前体和TTR等5种蛋白质在模型组心肌组织表达下调,MLC和HspB6等2种蛋白质在模型组表达上调。结果表明腹主动脉缩窄致大鼠心肌肥大后,心肌组织蛋白质组变化显著,这些变化涉及与心肌细胞能量代谢、细胞骨架以及心肌收缩等有关的几组蛋白质,提示上述蛋白质组改变可能参与了心肌肥大过程,并首次发现TTR在肥大心肌表达下调,其在心肌肥大发生中的作用有待于进一步研究。
Aim:To observe the expression of UII and its receptor in 2DM mouse ***:Blood glucose monitoring device was used to examine the concentration of fast blood *** assay method was used to examine the concentration of plas...
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Aim:To observe the expression of UII and its receptor in 2DM mouse ***:Blood glucose monitoring device was used to examine the concentration of fast blood *** assay method was used to examine the concentration of plasma UII and ***-PCR method was used to assay the expression of GPR14 mRNA in mouse *** method was used to assay UII immunological activity ex- pression in mouse ***:Compared with Con group,the concentration of fasting blood glucose,plasma insulin and plasma UII were increased in 2DM group;immunological activity of UII was strong positive expression in 2DM mouse liver;the expression of GPR14 mRNA was up-regulated in 2DM mouse ***:It is possible that the increasing expression of UII derived from liver is a source of plasma *** is unclear that the up- regulated expression of GPR14 mRNA in 2DM group and deserve further study.
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