Proteomic Profiling Exosomes from Vascular Smooth Muscle Cell.

Proteomic Profiling Exosomes from Vascular Smooth Muscle Cell.
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DOI:
10.1002/prca.201700097
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发表时间:
2018-09
期刊:
Proteomics. Clinical applications
影响因子:
--
通讯作者:
Wang L
Wang L
中科院分区:
其他
文献类型:
--
作者:
Qiu H;Shi S;Wang S;Peng H;Ding SJ;Wang L

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血管平滑肌细胞(VSMC)和内皮细胞(EC)相互沟通,协调血管的发育和稳态。外泌体是参与这种交流的一种介质。表征外泌体中的蛋白质是理解VSMC-EC串扰如何由外泌体介导的关键的第一步。人类vsmc来源的外泌体中的蛋白质使用基于纳米lc -MS/MS的蛋白质组学进行了分析。鉴定出的蛋白质进行基因本体分析。vsmc衍生的外泌体也被评估在体内的促血管生成活性。在vsmc衍生的外泌体中鉴定了459种蛋白质。基因本体分析显示,外泌体蛋白参与179个细胞组分、120个分子功能和337个生物过程,其中细胞-细胞粘附和血小板活化/凝固居首位。在体内血管生成实验中,vsmc衍生的外泌体没有显示出促血管生成活性,这表明vsmc衍生的外泌体的主要功能是维持血管稳态。这些分析获得了vsmc衍生外泌体中蛋白质的系统视图,揭示了外泌体在VSMC-EC通信中的潜在调节功能,并表明vsmc衍生外泌体介导的功能失调可能扰乱血管稳态,从而导致血管疾病。
Vascular smooth muscle cells (VSMC) and endothelial cells (EC) communicate mutually to coordinate vascular development and homeostasis. Exosomes are emerging as one type of the mediators involved in this communication. Characterizing proteins in the exosomes is the critical first step in understanding how the VSMC-EC crosstalk is mediated by exosomes. The proteins in the human VSMC-derived exosomes are profiled using nanoLC-MS/MS based proteomics. The identified proteins are subjected to gene ontology analysis. The VSMC-derived exosomes are also assessed for proangiogenic activity in vivo. Four hundred and fifty-nine proteins are identified in the VSMC-derived exosomes. Gene ontology analysis revealed that the exosome proteins are involved in 179 cellular components, 120 molecular functions, and 337 biological processes, with cell–cell adhesion and platelet activation/coagulation ranked at the top. VSMC-derived exosomes do not display a proangiogenic activity in the in vivo angiogenesis assay, suggesting that the major function of VSMC-derived exosomes is to maintain vessel homeostasis. The analyses obtained a systematic view of proteins in the VSMC-derived exosomes, revealed the potential regulatory functions of the exosome in VSMC-EC communication, and suggest that dysregulation of VSMC-derived exosome-mediated functions may disturb vessel homeostasis thereby contributing to vascular diseases.
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