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腺嘌呤核苷酸转运蛋白 1 的表达调节缺血心脏的免疫反应。

Adenine Nucleotide Translocase 1 Expression Modulates the Immune Response in Ischemic Hearts.

机构信息

Department of Cardiology, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin and Berlin Institute of Health, 12200 Berlin, Germany.

Institute of Health Center for Regenerative Therapies (BCRT), Charité-Universitätsmedizin Berlin, 13353 Berlin, Germany.

出版信息

Cells. 2021 Aug 19;10(8):2130. doi: 10.3390/cells10082130.

DOI:10.3390/cells10082130
PMID:34440901
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8393693/
Abstract

Adenine nucleotide translocase 1 (ANT1) transfers ATP and ADP over the mitochondrial inner membrane and thus supplies the cell with energy. This study analyzed the role of ANT1 in the immune response of ischemic heart tissue. Ischemic ANT1 overexpressing hearts experienced a shift toward an anti-inflammatory immune response. The shift was characterized by low interleukin (IL)-1β expression and M1 macrophage infiltration, whereas M2 macrophage infiltration and levels of IL-10, IL-4, and transforming growth factor (TGFβ) were increased. The modulated immune response correlated with high mitochondrial integrity, reduced oxidative stress, low left ventricular end-diastolic heart pressure, and a high survival rate. Isolated ANT1-transgenic (ANT1-TG) cardiomyocytes expressed low levels of pro-inflammatory cytokines such as IL-1α, tumor necrosis factor α, and TGFβ. However, they showed increased expression and cellular release of anti-inflammatory immunomodulators such as vascular endothelial growth factor. The secretome from ANT1-TG cardiomyocytes initiated stress resistance when applied to ischemic wild-type cardiomyocytes and endothelial cells. It additionally prevented macrophages from expressing pro-inflammatory cytokines. Additionally, ANT1 expression correlated with genes that are related to cytokine and growth factor pathways in hearts of patients with ischemic cardiomyopathy. In conclusion, ANT1-TG cardiomyocytes secrete soluble factors that influence ischemic cardiac cells and initiate an anti-inflammatory immune response in ischemic hearts.

摘要

腺嘌呤核苷酸转位酶 1（ANT1）将 ATP 和 ADP 转运穿过线粒体内膜，从而为细胞提供能量。本研究分析了 ANT1 在缺血性心脏组织免疫反应中的作用。缺血性 ANT1 过表达的心脏经历了向抗炎免疫反应的转变。这种转变的特征是白细胞介素（IL）-1β表达和 M1 巨噬细胞浸润降低，而 M2 巨噬细胞浸润和 IL-10、IL-4 和转化生长因子（TGFβ）水平增加。调节后的免疫反应与线粒体完整性高、氧化应激低、左心室舒张末期心脏压力低和存活率高相关。分离的 ANT1 转基因（ANT1-TG）心肌细胞表达低水平的促炎细胞因子，如 IL-1α、肿瘤坏死因子α和 TGFβ。然而，它们表现出抗炎免疫调节剂如血管内皮生长因子的表达和细胞释放增加。ANT1-TG 心肌细胞的分泌组在应用于缺血性野生型心肌细胞和内皮细胞时引发了应激抵抗。它还阻止巨噬细胞表达促炎细胞因子。此外，ANT1 表达与缺血性心肌病患者心脏中与细胞因子和生长因子途径相关的基因相关。总之，ANT1-TG 心肌细胞分泌的可溶性因子影响缺血性心脏细胞，并在缺血性心脏中引发抗炎免疫反应。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dd56/8393693/6272394f41ca/cells-10-02130-g008.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dd56/8393693/6272394f41ca/cells-10-02130-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dd56/8393693/d76c9c4b187a/cells-10-02130-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dd56/8393693/59d9dc755a8e/cells-10-02130-g002.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dd56/8393693/50b6added61f/cells-10-02130-g005.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dd56/8393693/6272394f41ca/cells-10-02130-g008.jpg

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