Biochemical and biophysical research communications · 2020
Neutrophil-derived exosome from systemic sclerosis inhibits the proliferation and migration of endothelial cells.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Li Liya, Zuo Xiaoxia, Xiao Yizhi, Liu Di, Luo Hui, Zhu Honglin
Аннотация
OBJECTIVES: Systemic sclerosis (SSc) is an autoimmune disease characterized by vasculopathy, inflammation, and extensive fibrosis in multiple organs. Exosomes (EXOs) are cell-derived vesicles contained various DNAs, RNAs and proteins, and play important roles in various diseases. Here, we aimed to investigate the roles of SSc EXOs in angiogenesis related mechanisms.
METHODS: EXOs were isolated from plasma, cultured peripheral blood mononuclear cells (PBMCs)/neutrophil supernatants, and identified by transmission electron microscopy. The expression of S100A8/A9 was measured by real-time PCR and ELISA. Proliferation, migration and scratch assays in human dermal microvascular endothelial cells (HDMECs) were used to study the EXOs influence.
RESULTS: Plasma and neutrophil EXOs from SSc patients can suppress the proliferation and migration of HDMECs. High levels of S100A8/A9 were found in SSc EXOs which derived from plasma, PBMCs and neutrophils. The expression of S100A8/A9 in neutrophil EXOs was higher than that in PBMC EXOs in SSc patients. The proliferation and migration of HDMECs were possibly inhibited by S100A8/A9 of neutrophil EXOs.
CONCLUSIONS: Neutrophil EXOs from SSc patients inhibits the proliferation and migration of HDMECs, S100A8/A9 might play an important role in this process.
METHODS: EXOs were isolated from plasma, cultured peripheral blood mononuclear cells (PBMCs)/neutrophil supernatants, and identified by transmission electron microscopy. The expression of S100A8/A9 was measured by real-time PCR and ELISA. Proliferation, migration and scratch assays in human dermal microvascular endothelial cells (HDMECs) were used to study the EXOs influence.
RESULTS: Plasma and neutrophil EXOs from SSc patients can suppress the proliferation and migration of HDMECs. High levels of S100A8/A9 were found in SSc EXOs which derived from plasma, PBMCs and neutrophils. The expression of S100A8/A9 in neutrophil EXOs was higher than that in PBMC EXOs in SSc patients. The proliferation and migration of HDMECs were possibly inhibited by S100A8/A9 of neutrophil EXOs.
CONCLUSIONS: Neutrophil EXOs from SSc patients inhibits the proliferation and migration of HDMECs, S100A8/A9 might play an important role in this process.