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首页> 外文期刊>Cell and Tissue Research >Angiotensin-converting enzyme 2 augments the effects of endothelial progenitor cells-exosomes on vascular smooth muscle cell phenotype transition
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Angiotensin-converting enzyme 2 augments the effects of endothelial progenitor cells-exosomes on vascular smooth muscle cell phenotype transition

机译：血管紧张素转化酶2增强内皮祖细胞 - 外泌体对血管平滑肌细胞表型转变的影响

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Phenotype transition of vascular smooth muscle cells (VSMCs) is implicated in vascular diseases. Angiotensin-converting enzyme 2 (ACE2) is a perspective cardiovascular target due to its ability of converting angiotensin (Ang II) to Ang (1-7). Our group recently showed that ACE2 can regulate the function of endothelial progenitor cell-derived exosomes (EPC-EXs). Here, we investigate whether ACE2 could affect the role of EPC-EXs on phenotype transition of VSMCs. After co-incubation with EXs released from EPC overexpressed ACE2 (EPC-EXs(ACE2)), the ACE2 level and Ang II/Ang (1-7), proliferation/migration, phenotype gene, cytokine and NF-kappa B level on VSMCs were assessed. To determine the EX uptake route, VSMCs were pretreated with inhibitors. We found that (1) EPC-EXs and EPC-EXs(ACE2)were uptaken by VSMCs dominantly through caveolin-dependent endocytosis. (2) EPC-EXs(ACE2)remarkably increased the ACE2 level and decreased Ang II/Ang (1-7) in VSMCs activated by Ang II, whereas EPC-EXs(ACE2)pretreated by proteinase A blocked this effect. (3) EPC-EXs(ACE2)had better effects than EPC-EXs on reducing proliferation/migration activities and cytokine (MCP-1, TNF-alpha) secretion of Ang II-activated VSMCs. (4) EPC-EXs attenuated Ang II-induced VSMC synthetic phenotype change as evidenced by upregulated expressions of calponin and a-SMA and downregulated expressions of CRBP-1 and MYH10, associated with a decreased NF-kappa B level. EPC-EXs(ACE2)augmented these effects, which were attenuated by ACE2 inhibitor (DX600). In conclusion, EPC-EXs(ACE2)reduced Ang II-induced VSMC phenotype change by conveying functional ACE2 to downregulate the activated NF-kappa B pathway.
机译：血管平滑肌细胞（VSMC）的表型转换与血管疾病有关。血管紧张素转换酶2（ACE2）具有将血管紧张素II（Ang II）转化为Ang（1-7）的能力，是一种很有前景的心血管靶点。我们的研究小组最近发现，ACE2可以调节内皮祖细胞源性外质体（EPC-EXs）的功能。在这里，我们研究了ACE2是否能影响血管平滑肌细胞表型转换中EPC-EXs的作用。与EPC过度表达的ACE2释放的EXs（EPC-EXs（ACE2））共同孵育后，评估血管平滑肌细胞上的ACE2水平和Ang II/Ang（1-7）、增殖/迁移、表型基因、细胞因子和NF-κB水平。为了确定EX摄取途径，用抑制剂预处理VSMC。我们发现（1）血管平滑肌细胞主要通过小窝蛋白依赖的内吞作用摄取EPC-EXs和EPC-EXs（ACE2）。（2） 在血管紧张素Ⅱ激活的血管平滑肌细胞中，EPC-EXs（ACE2）显著增加ACE2水平并降低AngⅡ/Ang（1-7），而蛋白酶A预处理的EPC-EXs（ACE2）则阻断了这种作用。（3） EPC-EXs（ACE2）对AngⅡ激活的血管平滑肌细胞的增殖/迁移活性和细胞因子（MCP-1，TNF-α）分泌的抑制作用优于EPC-EXs。（4） EPC-EXs减弱了Ang II诱导的VSMC合成表型变化，其表现为钙调素和a-SMA表达上调，CRBP-1和MYH10表达下调，与NF-κB水平降低相关。EPC EXs（ACE2）增强了这些效应，ACE2抑制剂（DX600）减弱了这些效应。总之，EPC-EXs（ACE2）通过输送功能性ACE2来下调激活的NF-κB通路，从而减少Ang II诱导的VSMC表型变化。

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