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首页> 外文期刊>Journal of cardiovascular translational research. >Roles and Mechanisms of TGR5 in the Modulation of CD4(+) T Cell Functions in Myocardial Infarction
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Roles and Mechanisms of TGR5 in the Modulation of CD4(+) T Cell Functions in Myocardial Infarction

机译:TGR5在心肌梗死CD4(+)T细胞功能调节中的作用及机制

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Bile acid receptor TGR5 has been proved to play protective roles in the process of myocardial infarction (MI). Recently, we found spleen weight of Tgr5(+/+) mice was increased at 7-day post-MI but not in Tgr5(-/-) mice. Since the spleen is one of the main resources of immune and inflammatory cells post-MI, we conducted flow cytometry analysis of multiple immune cells in the heart post-MI. It showed the recruitment of CD4(+) T cells and CD8(+) T cells was continuously more in the heart of Tgr5(-/-) mice post-MI until 7 days after MI. Furthermore, CD4-specific TGR5 depletion mice exhibited aggravated ischemic injury. The mRNA expressions of the markers of Th1 and Treg were upregulated in the heart of Tgr5(-/-) mice at 7-day post-MI. These results suggested TGR5 modulates CD4(+) T cell functions and subsets distribution in the heart, and plays protective roles in myocardial infarction.
机译:胆汁酸受体TGR5已被证明在心肌梗死(MI)过程中起保护作用。最近,我们发现 Tgr5(+/+) 小鼠的脾脏重量在心肌梗死后 7 天增加,但在 Tgr5(-/-) 小鼠中没有增加。由于脾脏是心肌梗死后免疫细胞和炎症细胞的主要来源之一,因此我们对心肌梗死后心脏中的多个免疫细胞进行了流式细胞术分析。结果显示,CD4(+)T细胞和CD8(+)T细胞在心肌梗死后Tgr5(-/-)小鼠心脏中的募集持续增加,直到心肌梗死后7天。此外,CD4特异性TGR5耗竭小鼠表现出加重的缺血性损伤。心肌梗死后 7 天,Th1 和 Treg 标志物的 mRNA 表达在 Tgr5(-/-) 小鼠心脏中上调。这些结果表明TGR5调节CD4(+)T细胞功能和心脏亚群分布,并在心肌梗死中起保护作用。

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