Inflammation-induced endothelial cell-derived extracellular vesicles modulate the cellular status of pericytes.

Inflammation-induced endothelial cell-derived extracellular vesicles modulate the cellular status of pericytes.
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DOI:
10.1038/srep08505
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发表时间:
2015-02-17
期刊:
影响因子:
4.6
通讯作者:
Sasahara M
Sasahara M
中科院分区:
综合性期刊3区
文献类型:
--
作者:
Yamamoto S;Niida S;Azuma E;Yanagibashi T;Muramatsu M;Huang TT;Sagara H;Higaki S;Ikutani M;Nagai Y;Takatsu K;Miyazaki K;Hamashima T;Mori H;Matsuda N;Ishii Y;Sasahara M

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Emerging lines of evidence have shown that extracellular vesicles (EVs) mediate cell-to-cell communication by exporting encapsulated materials, such as microRNAs (miRNAs), to target cells. Endothelial cell-derived EVs (E-EVs) are upregulated in circulating blood in different pathological conditions; however, the characteristics and the role of these E-EVs are not yet well understood. In vitro studies were conducted to determine the role of inflammation-induced E-EVs in the cell-to-cell communication between vascular endothelial cells and pericytes/vSMCs. Stimulation with inflammatory cytokines and endotoxin immediately induced release of shedding type E-EVs from the vascular endothelial cells, and flow cytometry showed that the induction was dose dependent. MiRNA array analyses revealed that group of miRNAs were specifically increased in the inflammation-induced E-EVs. E-EVs added to the culture media of cerebrovascular pericytes were incorporated into the cells. The E-EV-supplemented cells showed highly induced mRNA and protein expression of VEGF-B, which was assumed to be a downstream target of the miRNA that was increased within the E-EVs after inflammatory stimulation. The results suggest that E-EVs mediate inflammation-induced endothelial cell-pericyte/vSMC communication, and the miRNAs encapsulated within the E-EVs may play a role in regulating target cell function. E-EVs may be new therapeutic targets for the treatment of inflammatory diseases.
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