阻断胞外HSP70活性改善阿霉素诱导的小鼠心功能障碍和心肌重构
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摘要
心衰是多种心脏疾病的终末阶段,是由任何可以损伤心室充血或射血能力的结构或功能性的心脏疾病引起的心脏排血量不足,从而不能满足机体代谢所需的一种状态。心脏组织异常重构是高血压心脏病及心衰的核心病理改变,也是造成慢性心力衰竭的主要原因。心衰的发病率及死亡率很高,严重威胁人类的健康。目前,治疗心衰的方法很多,包括药物、手术及介入疗法等,但是大部分治疗心衰的药物只能在表面上改善患者的症状和延缓病情的发展,手术治疗的预后也较差。因此,在现阶段尝试寻找新的治疗心衰的药物作用靶点就显得尤为重要。
近几年的研究发现,免疫-炎症反应参与了心衰的发生发展,调节免疫反应可能会成为改变心衰进程的一种途径。损伤相关模式分子(DAMPs)是组织细胞在应激状态下以主动或被动方式释放到细胞外的一类物质,DAMPs既可以通过与模式识别受体结合,激活先天性免疫系统,启动或促进炎症反应,还可以通过调节获得性免疫反应的极化方向影响炎症的发展方向。本实验室前期的研究发现,细胞内和细胞外的热休克蛋白70(HSP70)对心脏组织免疫炎症反应发挥不同的调节作用,胞外HSP70可能作为一种DAMP分子调节组织的免疫反应。基于以上这些理论和研究结果,本文进一步对阻断胞外HSP70活性是否能够治疗心衰及可能的作用机制进行了探讨。我们采用了阿霉素引起的急性和慢性心衰动物模型及高血压心脏病模型进行实验和验证,结果发现,阿霉素引起心肌组织及血清中HSP70含量显著增加,且大量表达的HSP70主要分布于胞外及胞膜,利用HSP70中和性抗体(HSP70Ab)阻断胞外HSP70活性能够显著改善急性和慢性心衰小鼠心功能障碍和心肌重构。急性心衰小鼠心脏组织炎症反应被激活,浸润的中性粒细胞数量显著增多,并大量表达IL-6、IL-17等促炎细胞因子,而阻断胞外HSP70活性则在增加巨噬细胞数量的同时显著减少了中性粒细胞的浸润,显著减少了凋亡的中性粒细胞的数量和促炎细胞因子的表达,而使抗炎细胞因子如IL-10的含量显著增加,同时,HSP70Ab显著上调了具有促炎症转归作用的几种蛋白和脂质介质的表达,因此,我们认为阻断胞外HSP70活性正是通过促进心脏组织炎症的主动转归而发挥其治疗急性心衰的作用。自噬是免疫反应的重要的效应器,在慢性心衰中,阻断胞外HSP70活性显著减少了心脏组织活性氧自由基的含量,同时活化自噬,抑制心肌细胞老化,从而发挥对心肌组织的保护作用,改善心功能障碍和心肌重构。此外,我们还对三种促炎症转归脂质介质的具体细胞作用和胞外HSP70发挥作用的信号通路进行了初步研究,结果表明,脂氧素等脂质介质通过干预NFκB的入核而调节NFKB下游信号的活化；胞外HSP70可能主要与Toll样受体2(TLR2)相结合,活化TLR2下游信号通路,进而调节组织免疫-炎症反应。本研究不仅有助于深入理解免疫-炎症反应在心衰中的作用,同时也为开发新型的抗心衰药物提供了研究线索和潜在的靶点。
Heart failure (HF), which is characterized by progressive ventricular remodeling and functional impairment, is a common terminal phase of heart diseases induced by a variety of injuries. In the progress of HF, cardiac output fails to meet the need of body metabolism because of impairment of myocardial systolic and (or) diastolic function. The incidence rate of HF is gradually increasing. However, the drug therapy only ameliorates symptoms of patient with HF and prognosis of surgery is always poor. The approach in the medical treatment of HF is merely adequate, so the discovery of new drug target is extremely urgent.
Numerous evidences show that immune-inflammatory responses play an important role in the pathogenesis of HF. It might be a beneficial strategy to retard the progression of HF by immune modulation. Molecules of damage associated molecular patterns (DAMPs), which can be actively or passively released to the extracellular space, can ignite innate immune response by activating the pattern recognized receptors (for example, Toll like receptor), leading to inflammation response and tissue injury. Our previous research indicated that extracellular HSP70might act as a molecule of DAMP. We wondered if HSP70could induce immune response in the myocardium and participate in the pathogenesis of cardiac remodeling of HF. In this study, we explored the immune-stimulating activity of extracellular HSP70and blocked its activity by a specific anti-HSP70neutralizing antibody (HSP70Ab) to test whether inhibition of extra-HSP70activity could exert therapeutic efficiency against established cardiac remodeling and dysfunction induced by doxorubicin (Dox) and pressure overload. Our studies indicated that administration of Dox enhanced the level of HSP70in the myocardium and serum in mice and the most molecules of HSP70located in the membrane and extracellular space. Therapeutic blocking of extra-HSP70activity markedly attenuated Dox induced cardiac dysfunction and remodeling in acute and chronic HF. The inflammation responses were activated in the Dox-induced acute HF group, evidenced by increasing accumulation of neutrophils and expression of pro-inflammation mediators, including IL-6and IL-17. In contrast, functional blockage of extra-HSP70inhibited the accumulation of neutrophils in the myocardium and inhibited expression of pro-inflammatory mediators, whereas it elevated levels of anti-inflammation and pro-resolution mediators, including specific proteins and lipids. These results indicated that the cardiac protective effects of blocking extra-HSP70were largely attributed to its capability to regulate immune response and promote resolution of inflammation in the heart. Autophagy plays an important role in the immune regulation. Advanced studies indicated that functional blockage of extra-HSP70restored cardiac function and attenuated cardiac remodeling via mitigating oxidative stress, up-regulating autophagy activities and inhibiting cellular senescence in Dox-induced chronic HF in mice. Furthermore, our study indicated that extra-HSP70may act through combining with Toll-like receptor2and then activating its intracellular downstream signals. What's more, some pro-resolution mediators, such as LXA4, ProD1and RvD1, can significantly inhibit the ligand-stimulated NFκB activity through interfering with NFκB translocation from cytoplast to nucleus. Our study will contribute to understanding the roles of inflammation responses in myocardial injury and remodeling and provide research clues for the development of new anti-HF drugs.
近几年的研究发现,免疫-炎症反应参与了心衰的发生发展,调节免疫反应可能会成为改变心衰进程的一种途径。损伤相关模式分子(DAMPs)是组织细胞在应激状态下以主动或被动方式释放到细胞外的一类物质,DAMPs既可以通过与模式识别受体结合,激活先天性免疫系统,启动或促进炎症反应,还可以通过调节获得性免疫反应的极化方向影响炎症的发展方向。本实验室前期的研究发现,细胞内和细胞外的热休克蛋白70(HSP70)对心脏组织免疫炎症反应发挥不同的调节作用,胞外HSP70可能作为一种DAMP分子调节组织的免疫反应。基于以上这些理论和研究结果,本文进一步对阻断胞外HSP70活性是否能够治疗心衰及可能的作用机制进行了探讨。我们采用了阿霉素引起的急性和慢性心衰动物模型及高血压心脏病模型进行实验和验证,结果发现,阿霉素引起心肌组织及血清中HSP70含量显著增加,且大量表达的HSP70主要分布于胞外及胞膜,利用HSP70中和性抗体(HSP70Ab)阻断胞外HSP70活性能够显著改善急性和慢性心衰小鼠心功能障碍和心肌重构。急性心衰小鼠心脏组织炎症反应被激活,浸润的中性粒细胞数量显著增多,并大量表达IL-6、IL-17等促炎细胞因子,而阻断胞外HSP70活性则在增加巨噬细胞数量的同时显著减少了中性粒细胞的浸润,显著减少了凋亡的中性粒细胞的数量和促炎细胞因子的表达,而使抗炎细胞因子如IL-10的含量显著增加,同时,HSP70Ab显著上调了具有促炎症转归作用的几种蛋白和脂质介质的表达,因此,我们认为阻断胞外HSP70活性正是通过促进心脏组织炎症的主动转归而发挥其治疗急性心衰的作用。自噬是免疫反应的重要的效应器,在慢性心衰中,阻断胞外HSP70活性显著减少了心脏组织活性氧自由基的含量,同时活化自噬,抑制心肌细胞老化,从而发挥对心肌组织的保护作用,改善心功能障碍和心肌重构。此外,我们还对三种促炎症转归脂质介质的具体细胞作用和胞外HSP70发挥作用的信号通路进行了初步研究,结果表明,脂氧素等脂质介质通过干预NFκB的入核而调节NFKB下游信号的活化；胞外HSP70可能主要与Toll样受体2(TLR2)相结合,活化TLR2下游信号通路,进而调节组织免疫-炎症反应。本研究不仅有助于深入理解免疫-炎症反应在心衰中的作用,同时也为开发新型的抗心衰药物提供了研究线索和潜在的靶点。
Heart failure (HF), which is characterized by progressive ventricular remodeling and functional impairment, is a common terminal phase of heart diseases induced by a variety of injuries. In the progress of HF, cardiac output fails to meet the need of body metabolism because of impairment of myocardial systolic and (or) diastolic function. The incidence rate of HF is gradually increasing. However, the drug therapy only ameliorates symptoms of patient with HF and prognosis of surgery is always poor. The approach in the medical treatment of HF is merely adequate, so the discovery of new drug target is extremely urgent.
Numerous evidences show that immune-inflammatory responses play an important role in the pathogenesis of HF. It might be a beneficial strategy to retard the progression of HF by immune modulation. Molecules of damage associated molecular patterns (DAMPs), which can be actively or passively released to the extracellular space, can ignite innate immune response by activating the pattern recognized receptors (for example, Toll like receptor), leading to inflammation response and tissue injury. Our previous research indicated that extracellular HSP70might act as a molecule of DAMP. We wondered if HSP70could induce immune response in the myocardium and participate in the pathogenesis of cardiac remodeling of HF. In this study, we explored the immune-stimulating activity of extracellular HSP70and blocked its activity by a specific anti-HSP70neutralizing antibody (HSP70Ab) to test whether inhibition of extra-HSP70activity could exert therapeutic efficiency against established cardiac remodeling and dysfunction induced by doxorubicin (Dox) and pressure overload. Our studies indicated that administration of Dox enhanced the level of HSP70in the myocardium and serum in mice and the most molecules of HSP70located in the membrane and extracellular space. Therapeutic blocking of extra-HSP70activity markedly attenuated Dox induced cardiac dysfunction and remodeling in acute and chronic HF. The inflammation responses were activated in the Dox-induced acute HF group, evidenced by increasing accumulation of neutrophils and expression of pro-inflammation mediators, including IL-6and IL-17. In contrast, functional blockage of extra-HSP70inhibited the accumulation of neutrophils in the myocardium and inhibited expression of pro-inflammatory mediators, whereas it elevated levels of anti-inflammation and pro-resolution mediators, including specific proteins and lipids. These results indicated that the cardiac protective effects of blocking extra-HSP70were largely attributed to its capability to regulate immune response and promote resolution of inflammation in the heart. Autophagy plays an important role in the immune regulation. Advanced studies indicated that functional blockage of extra-HSP70restored cardiac function and attenuated cardiac remodeling via mitigating oxidative stress, up-regulating autophagy activities and inhibiting cellular senescence in Dox-induced chronic HF in mice. Furthermore, our study indicated that extra-HSP70may act through combining with Toll-like receptor2and then activating its intracellular downstream signals. What's more, some pro-resolution mediators, such as LXA4, ProD1and RvD1, can significantly inhibit the ligand-stimulated NFκB activity through interfering with NFκB translocation from cytoplast to nucleus. Our study will contribute to understanding the roles of inflammation responses in myocardial injury and remodeling and provide research clues for the development of new anti-HF drugs.
引文
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