Vesicle miR-195 derived from endothelial cells inhibits expression of serotonin transporter in vessel smooth muscle cells

Junzhong Gu, Huiyuan Zhang, Bingyang Ji, Hui Jiang, Tao Zhao, Rongcai Jiang, Zhiren Zhang, Shengjiang Tan, Asif Ahmed, Yuchun Gu*

*Corresponding author for this work

Research output: Contribution to journalArticle

Abstract

Serotonin or 5-hydroxytryptamine (5-HT) has been shown to be essential in lots of physiological and pathological processes. It is well known that 5-HT and 5-HT transporter (5-HTT) play important roles in the pulmonary artery in pulmonary hypertension. However, little is known about the function of 5-HTT in other arteries. In this study we found that the expression of 5-HTT was elevated in injured carotid arteries and over-expression of 5-HTT induced proliferation of smooth muscle cells (SMCs); however, this phenotype could be reversed by knocking-down of 5-HTT or endothelial cells conditional medium (EC-CM). A 5-HTT inhibitor, fluoxetine, treated animals also exhibited reduced restenosis after injury. We identified that miR-195 was packaged in the extracellular vesicles from EC-CM. We further confirmed that extracellular vesicles could transfer miR-195 from ECs to SMCs to inhibit the expression of 5-HTT in SMCs and the proliferation of SMCs. These results provide the first evidence that ECs communicate with SMCs via micro-RNA195 in the regulation of the proliferation of SMCs through 5-HTT, which will contribute to a better understanding of communications between ECs and SMCs via micro-RNA. Our findings suggest a potential target for the control of vessel restenosis.

Original languageEnglish
Article number43546
Number of pages10
JournalScientific Reports
Volume7
DOIs
Publication statusPublished - 8 Mar 2017

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Serotonin Plasma Membrane Transport Proteins
Smooth Muscle Myocytes
Serotonin
Endothelial Cells
Physiological Phenomena
Fluoxetine
Pathologic Processes
MicroRNAs
Carotid Arteries
Pulmonary Hypertension
Pulmonary Artery
Arteries
Cell Proliferation
Phenotype

Bibliographical note

This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license,
unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/

Funding: 973 Project No. 2013CB531206, 973 Project No.
2012CB517803 and NSF No.81170236, No.31127001

Cite this

Gu, Junzhong ; Zhang, Huiyuan ; Ji, Bingyang ; Jiang, Hui ; Zhao, Tao ; Jiang, Rongcai ; Zhang, Zhiren ; Tan, Shengjiang ; Ahmed, Asif ; Gu, Yuchun. / Vesicle miR-195 derived from endothelial cells inhibits expression of serotonin transporter in vessel smooth muscle cells. In: Scientific Reports. 2017 ; Vol. 7.
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abstract = "Serotonin or 5-hydroxytryptamine (5-HT) has been shown to be essential in lots of physiological and pathological processes. It is well known that 5-HT and 5-HT transporter (5-HTT) play important roles in the pulmonary artery in pulmonary hypertension. However, little is known about the function of 5-HTT in other arteries. In this study we found that the expression of 5-HTT was elevated in injured carotid arteries and over-expression of 5-HTT induced proliferation of smooth muscle cells (SMCs); however, this phenotype could be reversed by knocking-down of 5-HTT or endothelial cells conditional medium (EC-CM). A 5-HTT inhibitor, fluoxetine, treated animals also exhibited reduced restenosis after injury. We identified that miR-195 was packaged in the extracellular vesicles from EC-CM. We further confirmed that extracellular vesicles could transfer miR-195 from ECs to SMCs to inhibit the expression of 5-HTT in SMCs and the proliferation of SMCs. These results provide the first evidence that ECs communicate with SMCs via micro-RNA195 in the regulation of the proliferation of SMCs through 5-HTT, which will contribute to a better understanding of communications between ECs and SMCs via micro-RNA. Our findings suggest a potential target for the control of vessel restenosis.",
author = "Junzhong Gu and Huiyuan Zhang and Bingyang Ji and Hui Jiang and Tao Zhao and Rongcai Jiang and Zhiren Zhang and Shengjiang Tan and Asif Ahmed and Yuchun Gu",
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Vesicle miR-195 derived from endothelial cells inhibits expression of serotonin transporter in vessel smooth muscle cells. / Gu, Junzhong; Zhang, Huiyuan; Ji, Bingyang; Jiang, Hui; Zhao, Tao; Jiang, Rongcai; Zhang, Zhiren; Tan, Shengjiang; Ahmed, Asif; Gu, Yuchun.

In: Scientific Reports, Vol. 7, 43546, 08.03.2017.

Research output: Contribution to journalArticle

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AU - Zhao, Tao

AU - Jiang, Rongcai

AU - Zhang, Zhiren

AU - Tan, Shengjiang

AU - Ahmed, Asif

AU - Gu, Yuchun

N1 - This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/ Funding: 973 Project No. 2013CB531206, 973 Project No. 2012CB517803 and NSF No.81170236, No.31127001

PY - 2017/3/8

Y1 - 2017/3/8

N2 - Serotonin or 5-hydroxytryptamine (5-HT) has been shown to be essential in lots of physiological and pathological processes. It is well known that 5-HT and 5-HT transporter (5-HTT) play important roles in the pulmonary artery in pulmonary hypertension. However, little is known about the function of 5-HTT in other arteries. In this study we found that the expression of 5-HTT was elevated in injured carotid arteries and over-expression of 5-HTT induced proliferation of smooth muscle cells (SMCs); however, this phenotype could be reversed by knocking-down of 5-HTT or endothelial cells conditional medium (EC-CM). A 5-HTT inhibitor, fluoxetine, treated animals also exhibited reduced restenosis after injury. We identified that miR-195 was packaged in the extracellular vesicles from EC-CM. We further confirmed that extracellular vesicles could transfer miR-195 from ECs to SMCs to inhibit the expression of 5-HTT in SMCs and the proliferation of SMCs. These results provide the first evidence that ECs communicate with SMCs via micro-RNA195 in the regulation of the proliferation of SMCs through 5-HTT, which will contribute to a better understanding of communications between ECs and SMCs via micro-RNA. Our findings suggest a potential target for the control of vessel restenosis.

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