心脏重构过程心室应变与生存蛋白的相关性研究
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摘要
研究背景和目的心肌梗塞是临床上常见的疾病,心肌梗塞后心脏重构与致残和致死密切相关。心肌梗塞后发生一系列分子生物学改变参与心脏重构过程。许多生长因子和细胞因子均可诱导丝氨酸/苏氨酸激酶Pim-1,Pim-1进而在细胞信号传导中发挥重要作用。最近研究发现Pim-1在心肌细胞中是Akt下游重要的生存调节子。许多研究关注于Akt在心肌细胞中的保护作用,但Pim-1作为信号蛋白的心脏保护作用还有待阐明。为了探讨心肌梗塞后心脏重构的细胞分子生物学改变及其相关机制并重点对Pim-1在其中的作用进行探讨,本实验通过绵羊心肌梗塞后心脏重构的动物模型,克隆并测序绵羊Pim-1信使RNA,探讨Pim-1相关生存蛋白在重构心肌中与重构张力和心肌细胞凋亡的关系。
方法2007年受国家留学基金公派到美国马里兰大学,实行联合培养计划,对冠状动脉缺血性心脏病进行相关课题的研究,选择心肌梗塞后心脏重构的相关研究。采用Dorset雄性杂交绵羊13只,随机分为两组:未手术组(n=5)和手术组(n=8)。手术组采用直接缝扎冠状动脉造成心尖部25%心肌梗塞。采集血流动力学和超声心动图,使用超声微测量技术实时监测左室游离壁的运动和形变,计算收缩末期和舒张末期张力,并收集未手术组和手术组心肌梗塞后10周的左室游离壁心肌组织行HE染色,评价动物模型和心脏重构的区域性。采取手术组左室游离壁心肌组织,提取总RNA,行逆转录聚合酶链式反应合成cDNA,使用特异性引物扩增PIM-1信使RNA,以Sanger末端终止法测序,使用软件进行拼接和分析。采取未手术组和手术组心肌梗塞后10周的左室游离壁远离梗塞区和临近梗塞区心肌组织行实时定量PCR、Western Blot检测Pim-1相关生存蛋白在重构心肌中的转录和翻译水平,免疫共沉淀检测不同区域Pim-1与其降解途径中重要分子伴侣Hsp70、Hsp90的关系,免疫荧光染色显示Pim-1的分布,TUNEL检测细胞凋亡。
结果心肌梗塞后手术组实验动物左室收缩末期容积和左室舒张末期容积显著增加,射血分数显著降低,室壁运动异常长度及室壁运动异常长度与同切面心内膜周长的比值均显著增加,心率、血压、心输出量无显著性差异。收缩末期和舒张末期张力呈区域性分布,在心肌梗塞区、临近梗塞区与远离梗塞区之间有显著差异,收缩末期张力显著下降,舒张末期张力显著增加。克隆并测序绵羊PIM-1信使RNA1341bp,分析发现其使用两个不同的起始密码子编码分子量为33kD和44kD的Pim-1蛋白,与人类及其他哺乳动物有高度同源性,5'端非编码区对于PIM-1信使RNA翻译起重要作用。与未手术组相比,手术组临近梗塞区PIM-1 mRNA、全细胞和细胞质44kD、33kD Pim-1蛋白显著增加,远离梗塞区无明显增加;Pim-1上游调控蛋白Akt在手术组临近梗塞区显著增加,在远离梗塞区无明显增加;临近梗塞区与Pim-1结合的Hsp90和Hsp70的比值显著增加,远离梗塞区无明显变化;Pim-1下游关键的抗凋亡蛋白:Bcl-2 mRNA和蛋白在手术组临近梗区明显增加,Bcl-xL mRNA无明显变化,Bcl-xL蛋白临近梗塞区增加,磷酸化Bad(Ser112)蛋白在临近梗塞区明显增加,远离梗塞区均无明显变化;TUNEL阳性细胞数在临近梗塞区显著增加,远离梗塞区无明显增加。重构张力和对应的生存蛋白水平相关分析显示生存蛋白水平与重构张力呈显著正相关。
结论冠状动脉结扎术建立绵羊心肌梗塞后心脏重构动物模型,可作为单发中等大小的心肌梗塞后心脏重构代表性的动物模型。通过心室表面超声微探头阵列实时监测心脏重构发现心肌梗塞后心脏重构是不均一的,收缩末期张力和舒张末期(重构)张力存在区域性的差别。绵羊PIM-1信使RNA全编码区和部分非编码区以及翻译产物与人及其他哺乳动物有高度同源性,在进化上高度保守。它可使用两个不同的起始密码子编码分子量为33kD和44kD的Pim-1蛋白,5'端非编码区对于其翻译起重要作用。绵羊心脏重构模型中Pim-1水平受多种调节机制控制,Pim-1相关生存蛋白呈区域性分布,并与重构张力相关,但这种上调不足以保护心肌细胞免于凋亡。
创新和展望
1.首次成功建立绵羊心尖部中等大小心肌梗塞后心脏重构动物模型,展示了心肌梗塞后不均一的心脏重构过程;
2.首次克隆并测序绵羊PIM-1信使RNA;
3.首次发现了Pim-1及其相关生存蛋白呈重构张力相关性区域分布,并探讨了这种分布的分子机制。
今后的研究可以通过过表达或敲除Pim-1及其相关生存蛋白,进一步探讨它们参与心脏重构的分子机制。
Objective Myocardial infarction (MI) continues to be a major health care problem. Left ventriclular (LV) remodeling after MI is associated with disability and death. A cascade of molecular events is involved in the cardiac remodeling process post MI. The serine/threonine kinase Pim-1 plays a critical role in the transduction of mitogenic signals and is rapidly induced by a variety of growth factors and cytokines. Pim-1 was recently identified as a cardiomyocyte survival regulator downstream of Akt in the myocardium. The protective effects of Akt in the myocardium have been intensively studied; but the cardioprotective role of Pim-1 as a signaling protein has not been fully clarified. The present study aims to clone and sequence PIM-1 mRNA and examine the Pim-1 associated survival proteins and its association with the strains and apoptosis in the remodeling myocardium in a large animal model.
Methods Thirteen male Dorsett hybrid sheep bred for laboratory use were randomly divided to two groups: Non-MI(N=5) and MI(N=8). MI of 25% LV mass was created in MI group by ligation of coronary arterys. Echocardiograms and hemodynamic data were collected. The post-MI LV regional movement and deformation were monitored with sonomicrometry and quantified using areal end-systolic strain and remodeling strain. Total RNA was extracted from ovine heart tissues, and then first-strand cDNA was synthesized. The ovine PIM-1 cDNA was amplified by PCR using specific primers and PCR products were sequenced. Data were analyzed by softwares. Myocardial tissue samples were harvested at 10 weeks after MI from the remote and adjacent regions of the infarct for analyses of Pim-1 and Pim-1 associated survival signaling proteins and apoptosis.
Results Both the LVESV and the LVEDV increased significantly, while the EF decreased over 10 weeks after MI. An increase in the length of wall motion abnormality was observed. Likewise, the ratio of wall motion abnormality to endocardial circumference significantly increased. There is no statistically significant change in heart rate, mean arterial pressure, and cardiac output during the whole course of the study. The end-systolic strains of the infarct and the adjacent regions decreased significantly after MI, while the remodeling strains of the infarct and the adjacent regions increased significantly after MI. The cDNA (1341bp) of ovine Pim-1 with the coding sequences for two Pim-1 kinase isoforms, 33 and 44 kDa, was first identified. It is highly conserved. Its 5'-UTR is involved in translational regulation. Both the isoforms expressed in heart tissue and the overall Pim-1 expression were highly controlled at multiple molecular levels. Pim-1, as well as Pim-1 mediated survival signaling proteins, Bcl-2, Bcl-xL, and phospho-Bad (Ser112), were upregulated in the adjacent region at 10 weeks post-MI and correlated positively with the degree of the remodeling. The tissue from the adjacent region exhibited significant increase in Akt expression compared to that from the normal control tissue. The ratio of Hsp90 and Hsp70 bound to Pim-1 significantly increased in the tissue from the adjacent region compared to that in the normal control tissue. However, the apoptotic activities also increased with remodeling strain.
Conclusions The sheep MI model created by ligation of coronary arterys is a representative cardiac remodeling model. The sonomicrometry array showed that the process of remodeling is inhomogeneous and the end-systolic and remodeling strain are region-specific. PIM-1 mRNA is highly conserved and encodes 33kD and 44kD Pim-1 by utilizing alternative translation initiation codons. Its 5"-UTR is involved in translational regulation. Pim-1 is regulated in multiple levels. The adjacent region experienced higher remodeling strain and exhibited significant upregulation of Pim-1 related survival signals. A positive correlation between the survival proteins expressions and the regional remodeling strain is observed. The results suggest that following an MI, the myocytes in this region attempted to survive by increasing the expressions of the survival signals, however, the intrinsic elevations of the survival signals were not sufficient to protect myocytes from apoptosis.
方法2007年受国家留学基金公派到美国马里兰大学,实行联合培养计划,对冠状动脉缺血性心脏病进行相关课题的研究,选择心肌梗塞后心脏重构的相关研究。采用Dorset雄性杂交绵羊13只,随机分为两组:未手术组(n=5)和手术组(n=8)。手术组采用直接缝扎冠状动脉造成心尖部25%心肌梗塞。采集血流动力学和超声心动图,使用超声微测量技术实时监测左室游离壁的运动和形变,计算收缩末期和舒张末期张力,并收集未手术组和手术组心肌梗塞后10周的左室游离壁心肌组织行HE染色,评价动物模型和心脏重构的区域性。采取手术组左室游离壁心肌组织,提取总RNA,行逆转录聚合酶链式反应合成cDNA,使用特异性引物扩增PIM-1信使RNA,以Sanger末端终止法测序,使用软件进行拼接和分析。采取未手术组和手术组心肌梗塞后10周的左室游离壁远离梗塞区和临近梗塞区心肌组织行实时定量PCR、Western Blot检测Pim-1相关生存蛋白在重构心肌中的转录和翻译水平,免疫共沉淀检测不同区域Pim-1与其降解途径中重要分子伴侣Hsp70、Hsp90的关系,免疫荧光染色显示Pim-1的分布,TUNEL检测细胞凋亡。
结果心肌梗塞后手术组实验动物左室收缩末期容积和左室舒张末期容积显著增加,射血分数显著降低,室壁运动异常长度及室壁运动异常长度与同切面心内膜周长的比值均显著增加,心率、血压、心输出量无显著性差异。收缩末期和舒张末期张力呈区域性分布,在心肌梗塞区、临近梗塞区与远离梗塞区之间有显著差异,收缩末期张力显著下降,舒张末期张力显著增加。克隆并测序绵羊PIM-1信使RNA1341bp,分析发现其使用两个不同的起始密码子编码分子量为33kD和44kD的Pim-1蛋白,与人类及其他哺乳动物有高度同源性,5'端非编码区对于PIM-1信使RNA翻译起重要作用。与未手术组相比,手术组临近梗塞区PIM-1 mRNA、全细胞和细胞质44kD、33kD Pim-1蛋白显著增加,远离梗塞区无明显增加;Pim-1上游调控蛋白Akt在手术组临近梗塞区显著增加,在远离梗塞区无明显增加;临近梗塞区与Pim-1结合的Hsp90和Hsp70的比值显著增加,远离梗塞区无明显变化;Pim-1下游关键的抗凋亡蛋白:Bcl-2 mRNA和蛋白在手术组临近梗区明显增加,Bcl-xL mRNA无明显变化,Bcl-xL蛋白临近梗塞区增加,磷酸化Bad(Ser112)蛋白在临近梗塞区明显增加,远离梗塞区均无明显变化;TUNEL阳性细胞数在临近梗塞区显著增加,远离梗塞区无明显增加。重构张力和对应的生存蛋白水平相关分析显示生存蛋白水平与重构张力呈显著正相关。
结论冠状动脉结扎术建立绵羊心肌梗塞后心脏重构动物模型,可作为单发中等大小的心肌梗塞后心脏重构代表性的动物模型。通过心室表面超声微探头阵列实时监测心脏重构发现心肌梗塞后心脏重构是不均一的,收缩末期张力和舒张末期(重构)张力存在区域性的差别。绵羊PIM-1信使RNA全编码区和部分非编码区以及翻译产物与人及其他哺乳动物有高度同源性,在进化上高度保守。它可使用两个不同的起始密码子编码分子量为33kD和44kD的Pim-1蛋白,5'端非编码区对于其翻译起重要作用。绵羊心脏重构模型中Pim-1水平受多种调节机制控制,Pim-1相关生存蛋白呈区域性分布,并与重构张力相关,但这种上调不足以保护心肌细胞免于凋亡。
创新和展望
1.首次成功建立绵羊心尖部中等大小心肌梗塞后心脏重构动物模型,展示了心肌梗塞后不均一的心脏重构过程;
2.首次克隆并测序绵羊PIM-1信使RNA;
3.首次发现了Pim-1及其相关生存蛋白呈重构张力相关性区域分布,并探讨了这种分布的分子机制。
今后的研究可以通过过表达或敲除Pim-1及其相关生存蛋白,进一步探讨它们参与心脏重构的分子机制。
Objective Myocardial infarction (MI) continues to be a major health care problem. Left ventriclular (LV) remodeling after MI is associated with disability and death. A cascade of molecular events is involved in the cardiac remodeling process post MI. The serine/threonine kinase Pim-1 plays a critical role in the transduction of mitogenic signals and is rapidly induced by a variety of growth factors and cytokines. Pim-1 was recently identified as a cardiomyocyte survival regulator downstream of Akt in the myocardium. The protective effects of Akt in the myocardium have been intensively studied; but the cardioprotective role of Pim-1 as a signaling protein has not been fully clarified. The present study aims to clone and sequence PIM-1 mRNA and examine the Pim-1 associated survival proteins and its association with the strains and apoptosis in the remodeling myocardium in a large animal model.
Methods Thirteen male Dorsett hybrid sheep bred for laboratory use were randomly divided to two groups: Non-MI(N=5) and MI(N=8). MI of 25% LV mass was created in MI group by ligation of coronary arterys. Echocardiograms and hemodynamic data were collected. The post-MI LV regional movement and deformation were monitored with sonomicrometry and quantified using areal end-systolic strain and remodeling strain. Total RNA was extracted from ovine heart tissues, and then first-strand cDNA was synthesized. The ovine PIM-1 cDNA was amplified by PCR using specific primers and PCR products were sequenced. Data were analyzed by softwares. Myocardial tissue samples were harvested at 10 weeks after MI from the remote and adjacent regions of the infarct for analyses of Pim-1 and Pim-1 associated survival signaling proteins and apoptosis.
Results Both the LVESV and the LVEDV increased significantly, while the EF decreased over 10 weeks after MI. An increase in the length of wall motion abnormality was observed. Likewise, the ratio of wall motion abnormality to endocardial circumference significantly increased. There is no statistically significant change in heart rate, mean arterial pressure, and cardiac output during the whole course of the study. The end-systolic strains of the infarct and the adjacent regions decreased significantly after MI, while the remodeling strains of the infarct and the adjacent regions increased significantly after MI. The cDNA (1341bp) of ovine Pim-1 with the coding sequences for two Pim-1 kinase isoforms, 33 and 44 kDa, was first identified. It is highly conserved. Its 5'-UTR is involved in translational regulation. Both the isoforms expressed in heart tissue and the overall Pim-1 expression were highly controlled at multiple molecular levels. Pim-1, as well as Pim-1 mediated survival signaling proteins, Bcl-2, Bcl-xL, and phospho-Bad (Ser112), were upregulated in the adjacent region at 10 weeks post-MI and correlated positively with the degree of the remodeling. The tissue from the adjacent region exhibited significant increase in Akt expression compared to that from the normal control tissue. The ratio of Hsp90 and Hsp70 bound to Pim-1 significantly increased in the tissue from the adjacent region compared to that in the normal control tissue. However, the apoptotic activities also increased with remodeling strain.
Conclusions The sheep MI model created by ligation of coronary arterys is a representative cardiac remodeling model. The sonomicrometry array showed that the process of remodeling is inhomogeneous and the end-systolic and remodeling strain are region-specific. PIM-1 mRNA is highly conserved and encodes 33kD and 44kD Pim-1 by utilizing alternative translation initiation codons. Its 5"-UTR is involved in translational regulation. Pim-1 is regulated in multiple levels. The adjacent region experienced higher remodeling strain and exhibited significant upregulation of Pim-1 related survival signals. A positive correlation between the survival proteins expressions and the regional remodeling strain is observed. The results suggest that following an MI, the myocytes in this region attempted to survive by increasing the expressions of the survival signals, however, the intrinsic elevations of the survival signals were not sufficient to protect myocytes from apoptosis.
引文
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