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Research Article

血管紧张素II诱导的心肌细胞外泌体MiR-29a通过靶向VEGFA调节心脏微血管内皮细胞的增殖、迁移和血管生成

卷 22, 期 4, 2022

发表于: 01 April, 2022

页: [331 - 341] 页: 11

弟呕挨: 10.2174/1566523222666220303102951

价格: $65

摘要

背景:心肌细胞（cardiomyocytes ,CMs）释放的外泌体可能通过microRNA（miR）传递在血管生成中发挥重要作用。有研究报道miR-29a在调节血管生成和病理性心肌肥厚中发挥重要作用。然而，CMderived exosomal miR-29a是否参与调控心肌肥厚过程中心脏微血管内皮细胞（CMEC）的稳态尚未确定。 方法:用血管紧张素II（Ang II）诱导CM肥大，然后用超离心从CM条件培养基中提取外泌体。CMECs与条件培养基共培养，培养基中有或没有来自CMs的外泌体（nori -exos）或来自血管紧张素ii诱导的CMs的外泌体（Ang II-exos）。此外，使用感染miR-29a模拟物或抑制剂的CMs或CMECs进行拯救实验。然后进行试管形成实验、Transwell实验和5-乙炔基-20-脱氧尿苷（EdU）实验，以确定外泌体处理的CMECs的变化。采用qRT-PCR检测miR-29a的表达，Western blotting和流式细胞术检测CMECs的增殖情况。 结果:结果显示Ang ii诱导的外泌体miR-29a抑制CMECs的血管生成能力、迁移功能和增殖。随后，通过qRT-PCR和蛋白质印迹法检测miR-29a的下游靶基因血管内皮生长因子（vascular endothelial growth factor, VEGFA），结果证实miR-29a通过靶向抑制VEGFA的表达进而抑制CMECs的血管生成能力。 结论:我们的结果表明，来自Ang ii诱导的CMs的外泌体通过miR-29a转移到CMECs，靶向VEGFA，参与调控CMCE的增殖、迁移和血管生成。

关键词: 心肌细胞肥大，心肌细胞，心脏微血管内皮细胞，外泌体，miR-29a, VEGFA。

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