缺氧诱导的内皮细胞源性外泌体刺激血管平滑肌细胞增殖和迁移。

IF 1.3 4区 医学 Q4 MEDICINE, RESEARCH & EXPERIMENTAL
Qinggen Xiong, Fei Lu, Xiaoming Xie, Wei Zhou
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引用次数: 0

摘要

本研究主要利用体外培养的人VSMCs和体外培养的ECs,研究缺氧条件下外泌体(exosomes, Exos)是否参与ECs与VSMCs之间的通讯,并探讨ECs来源的外泌体在VSMCs异常增殖中的作用和机制。在低氧或常氧条件下单独培养VSMCs或共培养ECs,通过一系列细胞功能测定评估VSMCs的增殖和迁移。接下来,在缺氧或常氧条件下从ECs中提取外泌体并进行表征。随后,我们引入ECs-Exos观察其对VSMCs增殖和迁移的影响,并进一步评估转化生长因子- β受体1 (TGFBR1)途径相关蛋白的表达。最后,在ec中敲除TGFBR1后,评估ec - exos对VSMCs功能的影响。经ec - exos处理的VSMCs在缺氧环境下增殖和迁移能力增强,TGFBR1通路相关蛋白的表达上调。TGFβ1敲低的ec - exos明显逆转了ec - exos对缺氧条件下细胞增殖和迁移的促进作用。综上所述,缺氧影响内皮细胞分泌细胞外囊泡,其可被VSMCs内化,并通过传递TGFBR1加速VSMCs的异常增殖和迁移。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Hypoxia-induced endothelial cell-derived exosome stimulates vascular smooth muscle cell proliferation and migration.

This study mainly used human VSMCs and ECs cultured in vitro to investigate whether exosomes (Exos) are involved in the communication between ECs and VSMCs under hypoxia, and to explore the role and mechanism of ECs-derived exosomes in the abnormal proliferation of VSMCs. VSMCs proliferation and migration were assessed by a series of cell function assays after culturing VSMCs alone or co-culturing ECs under hypoxia or normoxia. Next, exosomes were extracted from ECs under hypoxia or normoxia and characterized. We then introduced ECs-Exos to observe their effects on VSMCs proliferation and migration, and further evaluated the expression of transforming growth factor-beta receptor 1 (TGFBR1) pathway-related proteins. Finally, the effect of ECs-Exos on VSMCs function was evaluated after knocking down TGFBR1 in ECs. VSMCs treated with ECs-Exos exhibited increased proliferation and migration ability in hypoxic environment, and the expression of TGFBR1 pathway-related proteins was upregulated. Administration of ECs-Exos with TGFβ1 knockdown conspicuously reversed the promoting effects of ECs-Exos on cell proliferation and migration under hypoxia. In summary, hypoxia affected the secretion of extracellular vesicles by endothelial cells, which can be internalized by VSMCs and accelerate the abnormal proliferation and migration of VSMCs by delivering TGFBR1.

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来源期刊
Biomedical Research-tokyo
Biomedical Research-tokyo 医学-医学:研究与实验
CiteScore
2.40
自引率
0.00%
发文量
19
审稿时长
>12 weeks
期刊介绍: Biomedical Research is peer-reviewed International Research Journal . It was first launched in 1990 as a biannual English Journal and later became triannual. From 2008 it is published in Jan-Apr/ May-Aug/ Sep-Dec..
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