Left ventricular hypertrophy is a common adaptive response to increased cardiac workload. Cardiomyocytes growth and increase in contractile force are conditioned by sufficient energy production, which implies appropriate mitochondrial function. The 60 kDa heat shock protein (HSP60) is a chaperone essential for mitochondrial proteostasis, but when translocates from mitochondria, it can also act as a potent inflammatory mediator binding to toll-like receptors (TLRs). In this study, we aimed to compare the expression pattern of HSP60, TLR2, and TLR4 in hypertrophic vs non-hypertrophic, normal human myocardium. We further examined whether HSP60 in situ binds to TLRs in hypertrophic myocardial tissue. In addition, expression of activated downstream targets of TLR 2/4 pathways was also evaluated.For this purpose, immunohistochemical expression analyses were performed on myocardial tissue samples obtained during the autopsy of human subjects in which left ventricular hypertrophy was the only cardiopathological finding and had died from sudden cardiac death, as well as from the subjects without any cardiac pathology, that died by unnatural death (accident or suicide). Double immunofluorescence was used to examine HSP60 translocation, while proximity ligation assay (PLA) was performed to assess HSP60 and TLRs interactions.Hypertrophic myocardium showed significantly higher expression of HSP60, TLR2, and TLR4 compared to normal myocardium. Furthermore, in hypertrophic cardiomyocytes, we found membrane translocation of HSP60 and signs of HSP60/TLR interactions.Conclusion: The obtained data point to an important supportive role of HSP60 in adaptive cardiomyocytes growth, while concomitant induction of TLR2 and TLR4 candidates HSP60-TLRs interactions as an early events during pathogenesis of secondary complications consequently to the left ventricular hypertrophy.

中文翻译：

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左心室肥大与心肌中HSP60，TLR2和TLR4的过度表达有关。

左心室肥大是对心脏负荷增加的常见适应性反应。心肌细胞的生长和收缩力的增加取决于产生足够的能量，这意味着适当的线粒体功能。60 kDa热休克蛋白（HSP60）是线粒体蛋白稳态所必需的分子伴侣，但是当从线粒体易位时，它也可以充当与toll样受体（TLR）结合的有效炎症介质。在这项研究中，我们旨在比较HSP60，TLR2和TLR4在肥厚性和非肥厚性正常人心肌中的表达模式。我们进一步检查了HSP60是否原位结合于肥厚性心肌组织中的TLR。此外，还评估了TLR 2/4途径激活的下游靶标的表达。免疫组织化学表达分析是针对在尸检过程中获得的心肌组织样本进行的，其中左心室肥大是唯一的心脏病理学发现，死于心源性猝死，以及死于无任何心脏病理学且死于非自然死亡的受试者（事故或自杀）。双重免疫荧光检测HSP60的转运，同时进行邻近结扎分析（PLA）评估HSP60和TLRs的相互作用。肥大型心肌的HSP60，TLR2和TLR4的表达明显高于正常心肌。此外，在肥厚型心肌细胞中，我们发现HSP60的膜易位以及HSP60 / TLR相互作用的迹象。