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Proteomic Profiling Exosomes from Vascular Smooth Muscle Cell
Author(s) -
Qiu Hong,
Shi Songshan,
Wang Shunchun,
Peng Hong,
Ding ShiJian,
Wang Lianchun
Publication year - 2018
Publication title -
proteomics – clinical applications
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.948
H-Index - 54
eISSN - 1862-8354
pISSN - 1862-8346
DOI - 10.1002/prca.201700097
Subject(s) - microvesicles , profiling (computer programming) , vascular smooth muscle , microbiology and biotechnology , computational biology , chemistry , biology , medicine , computer science , smooth muscle , microrna , biochemistry , operating system , gene
Purpose 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. Experimental design 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. Results 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. Conclusion and clinical relevance 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.