Peroxiredoxin 2 (PRDX2) is an antioxidant and molecular chaperone that can be secreted from tumor cells. But the role of PRDX2 in acute myocardial infarction (AMI) is not clear. In the current study, we demonstrate the role of PRDX2 from clinical trials, H9c2 cells and in a mouse model. ELISA analysis shows that serum concentrations of VEGF and inflammatory factor IL-1β, TNF-α and IL-6 were increased in AMI patients compared to a control group. The expression of PRDX2 was also upregulated. In vivo experiments show that the expression of PRDX2 inhibits hypoxia-induced oxidative stress injury to H9c2 cells. However, PRDX2 expression promotes TLR4 mediated inflammatory factor expression and VEGF expression under hypoxia conditions. PRDX2 overexpression in H9c2 cells also promotes human endothelial cell migration, vasculogenic mimicry formation and myocardial hypertrophy related protein expression. The overexpression of PRDX2 inhibits ROS level and myocardial injury after AMI but promotes inflammatory responses in vivo. Immunocytochemistry and immunofluorescence analysis show that overexpression of PRDX2 promotes angiogenesis and myocardial hypertrophy. Taken together, our results indicate that PRDX2 plays two roles in acute infarction - the promotion of cell survival and inflammatory myocardial hypertrophy.

中文翻译：

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急性心肌梗死中TLR4介导心肌肥大和生存中的PRDX2。

Peroxiredoxin 2（PRDX2）是一种抗氧化剂和分子伴侣，可以从肿瘤细胞中分泌出来。但是PRDX2在急性心肌梗死（AMI）中的作用尚不清楚。在当前的研究中，我们从临床试验，H9c2细胞和小鼠模型中证明PRDX2的作用。ELISA分析显示，与对照组相比，AMI患者的血清VEGF和炎性因子IL-1β，TNF-α和IL-6的浓度升高。PRDX2的表达也被上调。体内实验表明PRDX2的表达抑制了缺氧诱导的H9c2细胞的氧化应激损伤。但是，PRDX2表达促进缺氧条件下TLR4介导的炎症因子表达和VEGF表达。H9c2细胞中PRDX2的过表达也促进了人类内皮细胞的迁移，血管生成的拟态形成与心肌肥大相关的蛋白表达。PRDX2的过表达抑制AMI后ROS水平和心肌损伤，但在体内促进炎症反应。免疫细胞化学和免疫荧光分析表明PRDX2的过表达促进血管生成和心肌肥大。两者合计，我们的结果表明PRDX2在急性梗塞中起两个作用-促进细胞存活和炎症性心肌肥大。