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首页> 外文期刊>Cellular Physiology and Biochemistry >Transgenic Overexpression of IL-37 Protects Against Atherosclerosis and Strengthens Plaque Stability
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Transgenic Overexpression of IL-37 Protects Against Atherosclerosis and Strengthens Plaque Stability

机译：IL-37的转基因过表达可预防动脉粥样硬化并增强斑块稳定性

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Background/Aims Recently, studies have shown that interleukin-37 (IL-37) is involved in atherosclerosis-related diseases. However, the regulatory mechanisms of IL-37 in atherosclerosis remain unknown. This study aims to determine the role of IL-37 in atherosclerosis and to investigate the underlying mechanisms involved. Methods IL-37 expression in human atherosclerotic plaques was detected by immunohistochemical staining and real-time reverse transcription polymerase chain reaction (RT-PCR). Oil Red O staining was used to measure the size of plaques. Cell apoptosis in vitro and in vivo was tested by flow cytometric analysis and terminal deoxynucleotidyl-transferase mediated dUTP nick-end labeling (TUNEL) staining, respectively. Protein expression levels of IL-37, IL-18Rα and p-Smad3 were measured by Weston blotting. Results Immunohistochemical staining revealed that IL-37 was highly expressed in human atherosclerotic plaques. Intracellular cytokine staining revealed that infiltrated CD4+ T lymphocytes and vascular smooth muscle cells (VSMCs), but not macrophages, were the major sources of IL-37. Mice that overexpressed IL-37 exhibited significant improvements in their atherosclerotic burden, as demonstrated by reduced plaque size, increased collagen levels, and reduced numbers of apoptotic cells in vivo. Subsequently, mechanistic studies showed that IL-37 played an anti-atherosclerotic role, at least partially, through reducing inflammation by promoting the differentiation of the T helper cell anti-inflammatory phenotype, and through increasing plaque stability by decreasing matrix metalloproteinase (MMP)-2/13-mediated degradation of collagen and inhibiting VSMCs apoptosis. Conclusion IL-37 may be a novel potential therapeutic target in patients with atherosclerotic heart disease.
机译：背景/目的最近，研究表明白介素37（IL-37）与动脉粥样硬化相关疾病有关。但是，IL-37在动脉粥样硬化中的调节机制仍然未知。这项研究旨在确定IL-37在动脉粥样硬化中的作用，并调查涉及的潜在机制。方法通过免疫组织化学染色和实时逆转录聚合酶链反应（RT-PCR）检测人动脉粥样硬化斑块中IL-37的表达。油红O染色用于测量噬斑的大小。分别通过流式细胞术和末端脱氧核苷酸转移酶介导的dUTP缺口末端标记（TUNEL）染色测试了体外和体内细胞凋亡。通过Weston印迹法测量IL-37，IL-18Rα和p-Smad3的蛋白表达水平。结果免疫组织化学染色显示IL-37在人的动脉粥样硬化斑块中高表达。细胞内细胞因子染色显示，浸润的CD4 + T淋巴细胞和血管平滑肌细胞（VSMC）而非巨噬细胞是IL-37的主要来源。过表达IL-37的小鼠在动脉粥样硬化负担方面显示出显着改善，如斑块大小减小，胶原蛋白水平增加和体内凋亡细胞数量减少所证明。随后，机理研究表明，IL-37至少部分地通过促进T辅助细胞抗炎表型的分化来减少炎症，以及通过减少基质金属蛋白酶（MMP）-来增加斑块稳定性，从而至少部分地发挥抗动脉粥样硬化的作用。 2/13介导的胶原蛋白降解并抑制VSMCs凋亡。结论IL-37可能是治疗动脉粥样硬化性心脏病的新靶标。

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