钙转运异常与高尿酸导致的内皮细胞损伤的相关关系及其分子机制研究
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摘要
研究背景：随着我国社会的进步,居民蛋白摄入和果糖摄入的增多,高尿酸血症已经成为危害我国居民健康的一个重要的危险因素。随着研究的深入,学术界逐渐认识到,高尿酸(Uric acid, UA)导致的危害并不仅仅限于其能够导致痛风、泌尿系统结石和传统意义上的“尿酸性肾病”,人们发现,高UA本身就能够导致心血管系统和肾小球的损伤。其中高UA导致的内皮功能损伤和炎症反应起着重要的作用。目前认为,细胞内线粒体钙稳态失衡导致的线粒体功能损伤是内皮细胞损伤的主要机制之一,线粒体功能异常会直接导致细胞内活性氧(ROS)的产生增加,同时还会抑制内皮细胞内皮型一氧化氮合酶(eNOS)的产生以及一氧化氮(NO)的释放,此外还会导致细胞炎症因子产生的增多。因此,我们认为在高UA导致的内皮损伤过程中,可能也遵从这一途径,或者可能还有其他的特殊机制。这是本研究的出发点。
目的：探讨高UA导致的内皮损伤和炎症反应过程中细胞内钙启动机制。
方法：体外培养人脐静脉内皮细胞系(HUVEC-C),分别给予不同浓度和不同时间点的UA刺激。在本研究的第一部分,即UA刺激HUVEC-C后内皮损伤和炎症反应的现象研究中,针对细胞内不同部位的钙离子浓度,我们分别使用细胞胞浆钙离子([Ca2+]cyt)的特异性探针Fluo-3 AM和线粒体钙离子([Ca2+]mito)的特异性探针Rhod-2 AM,对活细胞进行染色,激光共聚焦显微镜观察细胞内钙离子的改变情况；针对细胞内的超氧阴离子(·O2-),我们使用细胞内总·O2-的特异性探针CM-H2DCFDA检测高UA刺激后的趋势,使用专门针对定位于线粒体·O2-的特异性探针——感染携带黄色荧光蛋白(cpYFP)的腺病毒的方法——检测线粒体内·O2-的变化；针对内皮损伤和炎症,我们使用硝酸还原酶法检测内皮细胞释放NO的改变趋势,逆转录-聚合酶链反应(RT-PCR)、Western Blot以及酶联免疫吸附法(ELISA)等方法分别检测eNOS以及一系列炎症因子如C-反应蛋白(CRP)、细胞间粘附分子-1(ICAM-1)和白介素-6(IL-6)在mRNA和蛋白水平表达的变化情况。在本研究的第二部分,即机制研究中,我们分别使用了一些常见的细胞内钙通道的特异性阻断剂,如细胞膜L型钙通道阻断剂Nicardipine,细胞膜钠钙交换体(NCXpm)的阻断剂KB-R7943；定位于线粒体的钙单向转运体(MCU)的阻断刺Ru360,线粒体钠钙交换体(NCXmito)的阻断剂CGP-37157;定位于内质网(ER)的月几浆网／内质网钙ATP酶(SERCA)的阻断剂Thapsigangin,1,4,5-三磷酸肌醇受体(IP3R)的阻断剂2APB以及Ryanodine受体的阻断剂Ryanodine(大剂量),阻断各自的钙通道,然后观察高UA刺激内皮细胞后内皮功能的变化以及炎症反应的改变趋势。
结果：高UA可呈时间、浓度依赖性地导致内皮损伤,表现为eNOS产生和NO释放的减少,预先使用ROS的清除剂维生素C (Vit C)有助于减轻其内皮损伤；在此过程中,[Ca2+]mito显著升高,而[Ca2+]cyt未出现显著变化;同时,内皮细胞产生·O2-显著增多,炎症因子释放明显增多。当阻断位于ER的IP3R和位于线粒体的NCXmito时,UA导致的内皮细胞[Ca2+]mito,总·O2-水平和线粒体·O2-水平均明显缓解,同时NO释放的降低会得到恢复,炎症因子的产生增多显著下降;而阻断SERCA和MCU则只能降低[Ca2+]mito和总·O2-水平的增加,无助于减少线粒体·O2-,也无减轻内皮损伤和炎症反应的作用。L型通道的阻断剂Nicardipine虽然不能减轻[Ca2+]mito,总·O2-水平和线粒体·O2-水平的增加,却能在一定程度上减轻内皮损伤和炎症。
结论：UA导致的内皮细胞损伤和炎症反应过程中,细胞内钙的变化,尤其是[Ca2+]mito的增多(线粒体钙超载)起着启动作用；ROS,尤其是·O2-的增多在此过程中起重要的介导作用；钙在IP3R和NCXmito两个通道的转运可能在此过程中起着重要的作用。本研究的结果揭示了UA导致内皮损伤的分子机制,有可能为临床治疗提供新的思路和靶点。
Background:Hyperuricemia has become an important risk factor for health of residents in China during the past 30 years. Researchers have recognized that the harmful of uric acid (UA) is not limited in its causing gout, urinary stones, and so called "uric acid nephropathy" only, on the contrary, it was found that UA per se is a risk factor in cardiovascular and renal damage, in which endothelial dysfunction plays a critical role. In the process of endothelial dysfunction, mitochondrial calcium homeostasis imbalance can increased intracellular reactive oxygen species (ROS) production, inhibit endothelial nitric oxide synthase (eNOS) production and nitric oxide (NO) release, and lead to increased inflammatory cytokine production. As a result, the main purpose of this study is to clarify whether UA induced endothelial injury and inflammation were also caused by this classical process, or have another special mechanism.
Objective:To investigate the mechanisms of intracellular calcium in the process of UA induced endothelial dysfunction and inflammation.
Methods:Human umbilical vein endothelial cells (HUVEC-C) cultured in vitro were stimulated with UA in different concentrations and different time points. The cytoplasmic calcium ([Ca2+]cyt) specific probe, Fluo-3 AM, and the mitochondrial calcium ([Ca2+]mito) specific probe, Rhod-2 AM, were employed to study the intracellular calcium changing after the UA stimulation, using confocal laser microscopy. The intracellular superoxide anion (·O2-) specific probe CM-H2DCFDA were employed to detect the changes in total·O2-, and the mitochondria·O2- specific probe, cpYFP, to detect the mitochondrial·O2-changes. Furthermore, we used reverse transcription-polymerase chain reaction (RT-PCR), Western Blot and enzyme-linked immunosorbent assay (ELISA) to detect eNOS and a series of inflammatory factors such as C-reactive protein (CRP), intercellular adhesion molecule-1 (ICAM-1) and interleukin-6 (IL-6) in mRNA and protein levels expression, respectively. In the second part of this study, different specific blockers for intracellular calcium channels were employed to inhibit the transduction through these channels. These blockers are, Nicardipine for L-type calcium channel, KB-R7943 for plasma membrane Na+/Ca2+exchanger (NCXpm), Ru360 for mitochondrial calcium uniporter (MCU), CGP-37157 for mitochondrial Na+/Ca2+exchanger (NCXmito), Thapsigangin for sarcoplasmic reticulum/endoplasmic reticulum calcium ATPase (SERCA),2-APB for 1,4,5-triphosphate receptor (IP3R), and high dose of Ryanodine for Ryanodine receptor (RyR).
Results:High concentration of UA induced endothelial dysfunction in a time and concentration dependent manner, marked as reduced eNOS production and NO release. In this process, [Ca2+]mito was significantly increased, while [Ca2+]cyt did not changed; ROS production was significantly increased, so as the release of inflammatory factors. When the blockers for IP3R and NCXmito were used, UA induced [Ca2+]mito, total·O2-levels and mitochondrial·O2-elevations were significantly decreased, while the reduction of NO release increased, and the elevated inflammatory factors generation were significantly decreased. However, when SERCA and MCU were blocked, we only observed the reduction of elevation of the [Ca2+]mito and the total·O2-levels, but not the protection effect for the endothelial dysfunction and inflammation.
Conclusion:High concentration of UA can induce endothelial dysfunction and inflammation, in which the the [Ca2+]mito were increased significantly (mitochondrial calcium overload). ROS, in particular,·O2-production, plays a mediating role in this process. Calcium transport through IP3R and NCXmito may play an important role. The results of this study clarified the molecular mechanisms of UA induced endothelial dysfunction and inflammation, and may provide a new target for clinics.
目的：探讨高UA导致的内皮损伤和炎症反应过程中细胞内钙启动机制。
方法：体外培养人脐静脉内皮细胞系(HUVEC-C),分别给予不同浓度和不同时间点的UA刺激。在本研究的第一部分,即UA刺激HUVEC-C后内皮损伤和炎症反应的现象研究中,针对细胞内不同部位的钙离子浓度,我们分别使用细胞胞浆钙离子([Ca2+]cyt)的特异性探针Fluo-3 AM和线粒体钙离子([Ca2+]mito)的特异性探针Rhod-2 AM,对活细胞进行染色,激光共聚焦显微镜观察细胞内钙离子的改变情况；针对细胞内的超氧阴离子(·O2-),我们使用细胞内总·O2-的特异性探针CM-H2DCFDA检测高UA刺激后的趋势,使用专门针对定位于线粒体·O2-的特异性探针——感染携带黄色荧光蛋白(cpYFP)的腺病毒的方法——检测线粒体内·O2-的变化；针对内皮损伤和炎症,我们使用硝酸还原酶法检测内皮细胞释放NO的改变趋势,逆转录-聚合酶链反应(RT-PCR)、Western Blot以及酶联免疫吸附法(ELISA)等方法分别检测eNOS以及一系列炎症因子如C-反应蛋白(CRP)、细胞间粘附分子-1(ICAM-1)和白介素-6(IL-6)在mRNA和蛋白水平表达的变化情况。在本研究的第二部分,即机制研究中,我们分别使用了一些常见的细胞内钙通道的特异性阻断剂,如细胞膜L型钙通道阻断剂Nicardipine,细胞膜钠钙交换体(NCXpm)的阻断剂KB-R7943；定位于线粒体的钙单向转运体(MCU)的阻断刺Ru360,线粒体钠钙交换体(NCXmito)的阻断剂CGP-37157;定位于内质网(ER)的月几浆网／内质网钙ATP酶(SERCA)的阻断剂Thapsigangin,1,4,5-三磷酸肌醇受体(IP3R)的阻断剂2APB以及Ryanodine受体的阻断剂Ryanodine(大剂量),阻断各自的钙通道,然后观察高UA刺激内皮细胞后内皮功能的变化以及炎症反应的改变趋势。
结果：高UA可呈时间、浓度依赖性地导致内皮损伤,表现为eNOS产生和NO释放的减少,预先使用ROS的清除剂维生素C (Vit C)有助于减轻其内皮损伤；在此过程中,[Ca2+]mito显著升高,而[Ca2+]cyt未出现显著变化;同时,内皮细胞产生·O2-显著增多,炎症因子释放明显增多。当阻断位于ER的IP3R和位于线粒体的NCXmito时,UA导致的内皮细胞[Ca2+]mito,总·O2-水平和线粒体·O2-水平均明显缓解,同时NO释放的降低会得到恢复,炎症因子的产生增多显著下降;而阻断SERCA和MCU则只能降低[Ca2+]mito和总·O2-水平的增加,无助于减少线粒体·O2-,也无减轻内皮损伤和炎症反应的作用。L型通道的阻断剂Nicardipine虽然不能减轻[Ca2+]mito,总·O2-水平和线粒体·O2-水平的增加,却能在一定程度上减轻内皮损伤和炎症。
结论：UA导致的内皮细胞损伤和炎症反应过程中,细胞内钙的变化,尤其是[Ca2+]mito的增多(线粒体钙超载)起着启动作用；ROS,尤其是·O2-的增多在此过程中起重要的介导作用；钙在IP3R和NCXmito两个通道的转运可能在此过程中起着重要的作用。本研究的结果揭示了UA导致内皮损伤的分子机制,有可能为临床治疗提供新的思路和靶点。
Background:Hyperuricemia has become an important risk factor for health of residents in China during the past 30 years. Researchers have recognized that the harmful of uric acid (UA) is not limited in its causing gout, urinary stones, and so called "uric acid nephropathy" only, on the contrary, it was found that UA per se is a risk factor in cardiovascular and renal damage, in which endothelial dysfunction plays a critical role. In the process of endothelial dysfunction, mitochondrial calcium homeostasis imbalance can increased intracellular reactive oxygen species (ROS) production, inhibit endothelial nitric oxide synthase (eNOS) production and nitric oxide (NO) release, and lead to increased inflammatory cytokine production. As a result, the main purpose of this study is to clarify whether UA induced endothelial injury and inflammation were also caused by this classical process, or have another special mechanism.
Objective:To investigate the mechanisms of intracellular calcium in the process of UA induced endothelial dysfunction and inflammation.
Methods:Human umbilical vein endothelial cells (HUVEC-C) cultured in vitro were stimulated with UA in different concentrations and different time points. The cytoplasmic calcium ([Ca2+]cyt) specific probe, Fluo-3 AM, and the mitochondrial calcium ([Ca2+]mito) specific probe, Rhod-2 AM, were employed to study the intracellular calcium changing after the UA stimulation, using confocal laser microscopy. The intracellular superoxide anion (·O2-) specific probe CM-H2DCFDA were employed to detect the changes in total·O2-, and the mitochondria·O2- specific probe, cpYFP, to detect the mitochondrial·O2-changes. Furthermore, we used reverse transcription-polymerase chain reaction (RT-PCR), Western Blot and enzyme-linked immunosorbent assay (ELISA) to detect eNOS and a series of inflammatory factors such as C-reactive protein (CRP), intercellular adhesion molecule-1 (ICAM-1) and interleukin-6 (IL-6) in mRNA and protein levels expression, respectively. In the second part of this study, different specific blockers for intracellular calcium channels were employed to inhibit the transduction through these channels. These blockers are, Nicardipine for L-type calcium channel, KB-R7943 for plasma membrane Na+/Ca2+exchanger (NCXpm), Ru360 for mitochondrial calcium uniporter (MCU), CGP-37157 for mitochondrial Na+/Ca2+exchanger (NCXmito), Thapsigangin for sarcoplasmic reticulum/endoplasmic reticulum calcium ATPase (SERCA),2-APB for 1,4,5-triphosphate receptor (IP3R), and high dose of Ryanodine for Ryanodine receptor (RyR).
Results:High concentration of UA induced endothelial dysfunction in a time and concentration dependent manner, marked as reduced eNOS production and NO release. In this process, [Ca2+]mito was significantly increased, while [Ca2+]cyt did not changed; ROS production was significantly increased, so as the release of inflammatory factors. When the blockers for IP3R and NCXmito were used, UA induced [Ca2+]mito, total·O2-levels and mitochondrial·O2-elevations were significantly decreased, while the reduction of NO release increased, and the elevated inflammatory factors generation were significantly decreased. However, when SERCA and MCU were blocked, we only observed the reduction of elevation of the [Ca2+]mito and the total·O2-levels, but not the protection effect for the endothelial dysfunction and inflammation.
Conclusion:High concentration of UA can induce endothelial dysfunction and inflammation, in which the the [Ca2+]mito were increased significantly (mitochondrial calcium overload). ROS, in particular,·O2-production, plays a mediating role in this process. Calcium transport through IP3R and NCXmito may play an important role. The results of this study clarified the molecular mechanisms of UA induced endothelial dysfunction and inflammation, and may provide a new target for clinics.
引文
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