Anti-inflammatory Gold-Induced Autologous Cytokines treatment triggers heart failure after myocardial infarction.

Discoveries (Craiova, Romania) Pub Date : 2017-12-31 DOI:10.15190/d.2017.10

Franziska Cordes, Adelina Curaj, Sakine Simsekyilmaz, Ulrich Schneider, Elisa A Liehn

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Abstract

Background: Gold-induced autologous cytokine (GOLDIC) treatment is usually used in the therapy of the inflammatory musculoskeletal disorders (e.g. osteoarthritis in humans) and is able to modulate the inflammatory reaction. Moreover, governed by chemokines and cytokines, the complex inflammatory response after an acute myocardial infarction (MI), the main cause of death worldwide, plays an important role in the preservation of heart function. Therefore, we hypothesized that GOLDIC could also have an important role in ventricular remodeling after MI.

Methods: Myocardial infarction was induced in mice and GOLDIC-enriched serum was directly injected directly in the infarcted tissue. Four weeks later, the function of the heart, as well as the infarction size and the scar composition were analyzed. Statistical analysis was performed with Prism 6.1 software (GraphPad), using 1-way ANOVA, followed by Newman-Keuls post-hoc-test, as indicated. Data are represented as mean ± SEM.

Results: Four weeks after MI, GOLDIC-treated mice show significantly decreased heart function and higher infarction size compared to the control group. Immunohistochemistry reveals a significantly increased number of myofibroblasts, correlating with higher collagen content in the infarcted area. Despite impaired heart function, angiogenesis in the GOLDIC-treated group is improved compared with the control, due to the increased vascular endothelial growth factor (VEGF) in the GOLDIC serum.

Conclusions: In conclusion, GOLDIC treatment impairs the ventricular remodeling, worsening the heart function. Therefore, these systemic effects should be taken into account when new therapies are designed for the musculoskeletal disorders.

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金诱导自体细胞因子抗炎治疗引发心肌梗塞后心力衰竭。

背景：金诱导自体细胞因子（GOLDIC）疗法通常用于治疗炎症性肌肉骨骼疾病（如人类骨关节炎），能够调节炎症反应。此外，在趋化因子和细胞因子的作用下，急性心肌梗塞（MI）后的复杂炎症反应在保护心脏功能方面发挥着重要作用。因此，我们假设 GOLDIC 也可能在心肌梗死后的心室重塑中发挥重要作用：方法：诱导小鼠心肌梗死，将富含 GOLDIC 的血清直接注射到梗死组织中。方法：诱导小鼠心肌梗死，将富含 GOLDIC 的血清直接注射到梗死组织中，四周后分析心脏功能、梗死面积和瘢痕成分。使用 Prism 6.1 软件（GraphPad）进行统计分析，采用单因素方差分析，然后进行纽曼-凯尔斯（Newman-Keuls）事后检验。数据以均数 ± SEM 表示：与对照组相比，心肌梗死四周后，经 GOLDIC 处理的小鼠心脏功能明显下降，梗死面积增大。免疫组化显示，肌成纤维细胞数量明显增加，这与梗死区域胶原蛋白含量较高有关。尽管心脏功能受损，但与对照组相比，GOLDIC治疗组的血管生成得到了改善，这是因为GOLDIC血清中的血管内皮生长因子（VEGF）增加了：总之，GOLDIC 治疗会损害心室重塑，恶化心脏功能。因此，在设计治疗肌肉骨骼疾病的新疗法时，应考虑到这些全身性影响。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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