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

Seiji Yamamoto; Shumpei Niida; Erika Azuma; Tsutomu Yanagibashi; Masashi Muramatsu; Ting Ting Huang; Hiroshi Sagara; Sayuri Higaki; Masashi Ikutani; Yoshinori Nagai; Kiyoshi Takatsu; Kenji Miyazaki; Takeru Hamashima; Hisashi Mori; Naoyuki Matsuda; Yoko Ishii; Masakiyo Sasahara

doi:10.1038/srep08505

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

Seiji Yamamoto^*, Shumpei Niida, Erika Azuma, Tsutomu Yanagibashi, Masashi Muramatsu, Ting Ting Huang, Hiroshi Sagara, Sayuri Higaki, Masashi Ikutani, Yoshinori Nagai, Kiyoshi Takatsu, Kenji Miyazaki, Takeru Hamashima, Hisashi Mori, Naoyuki Matsuda, Yoko Ishii, Masakiyo Sasahara

^*Corresponding author for this work

Research output: Contribution to journal › Article › peer-review

134 Scopus citations

Abstract

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.

Original language	English
Article number	8505
Journal	Scientific Reports
Volume	5
DOIs	https://doi.org/10.1038/srep08505
State	Published - 2014

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Yamamoto, S., Niida, S., Azuma, E., Yanagibashi, T., Muramatsu, M., Huang, T. T., Sagara, H., Higaki, S., Ikutani, M., Nagai, Y., Takatsu, K., Miyazaki, K., Hamashima, T., Mori, H., Matsuda, N., Ishii, Y., & Sasahara, M. (2014). Inflammation-induced endothelial cell-derived extracellular vesicles modulate the cellular status of pericytes. Scientific Reports, 5, Article 8505. https://doi.org/10.1038/srep08505

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title = "Inflammation-induced endothelial cell-derived extracellular vesicles modulate the cellular status of pericytes",

abstract = "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.",

author = "Seiji Yamamoto and Shumpei Niida and Erika Azuma and Tsutomu Yanagibashi and Masashi Muramatsu and Huang, {Ting Ting} and Hiroshi Sagara and Sayuri Higaki and Masashi Ikutani and Yoshinori Nagai and Kiyoshi Takatsu and Kenji Miyazaki and Takeru Hamashima and Hisashi Mori and Naoyuki Matsuda and Yoko Ishii and Masakiyo Sasahara",

note = "Publisher Copyright: {\textcopyright} 2015 Macmillan Publishers Limited.",

year = "2014",

doi = "10.1038/srep08505",

language = "英語",

volume = "5",

journal = "Scientific Reports",

issn = "2045-2322",

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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 2014, 'Inflammation-induced endothelial cell-derived extracellular vesicles modulate the cellular status of pericytes', Scientific Reports, vol. 5, 8505. https://doi.org/10.1038/srep08505

TY - JOUR

T1 - Inflammation-induced endothelial cell-derived extracellular vesicles modulate the cellular status of pericytes

AU - Yamamoto, Seiji

AU - Niida, Shumpei

AU - Azuma, Erika

AU - Yanagibashi, Tsutomu

AU - Muramatsu, Masashi

AU - Huang, Ting Ting

AU - Sagara, Hiroshi

AU - Higaki, Sayuri

AU - Ikutani, Masashi

AU - Nagai, Yoshinori

AU - Takatsu, Kiyoshi

AU - Miyazaki, Kenji

AU - Hamashima, Takeru

AU - Mori, Hisashi

AU - Matsuda, Naoyuki

AU - Ishii, Yoko

AU - Sasahara, Masakiyo

PY - 2014

Y1 - 2014

N2 - 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.

AB - 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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U2 - 10.1038/srep08505

DO - 10.1038/srep08505

M3 - 学術論文

C2 - 25687367

AN - SCOPUS:84923368860

SN - 2045-2322

VL - 5

JO - Scientific Reports

JF - Scientific Reports

M1 - 8505

ER -

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

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