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Platelet-derived microvesicles induce calcium oscillations and promote VSMC migration via TRPV4
Rationale: Abnormal migration of vascular smooth muscle cells (VSMCs) from the media to the interior is a critical process during the intimal restenosis caused by vascular injury. Here, we determined the role of platelet-derived microvesicles (PMVs) released by activated platelets in VSMC migration....
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Ivyspring International Publisher
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7797689/ https://www.ncbi.nlm.nih.gov/pubmed/33500733 http://dx.doi.org/10.7150/thno.47182 |
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author | Li, Shan-Shan Gao, Shuang Chen, Yi Bao, Han Li, Zi-Tong Yao, Qing-Ping Liu, Ji-Ting Wang, Yingxiao Qi, Ying-Xin |
author_facet | Li, Shan-Shan Gao, Shuang Chen, Yi Bao, Han Li, Zi-Tong Yao, Qing-Ping Liu, Ji-Ting Wang, Yingxiao Qi, Ying-Xin |
author_sort | Li, Shan-Shan |
collection | PubMed |
description | Rationale: Abnormal migration of vascular smooth muscle cells (VSMCs) from the media to the interior is a critical process during the intimal restenosis caused by vascular injury. Here, we determined the role of platelet-derived microvesicles (PMVs) released by activated platelets in VSMC migration. Methods: A percutaneous transluminal angioplasty balloon dilatation catheter was used to establish vascular intimal injury. Collagen I was used to activate PMVs, mimicking collagen exposure during intimal injury. To determine the effects of PMVs on VSMC migration in vitro, scratch wound healing assays were performed. Fluorescence resonance energy transfer was used to detect variations of calcium dynamics in VSMCs. Results: Morphological results showed that neointimal hyperplasia was markedly increased after balloon injury of the carotid artery in rats, and the main component was VSMCs. PMVs significantly promoted single cell migration and wound closure in vitro. Fluorescence resonance energy transfer revealed that PMVs induced temporal and dynamic calcium oscillations in the cytoplasms of VSMCs. The influx of extracellular calcium, but not calcium from intracellular stores, was involved in the process described above. The channel antagonist GSK219 and specific siRNA revealed that a membrane calcium channel, transient receptor potential vanilloid 4 (TRPV4), participated in the calcium oscillations and VSMC migration induced by PMVs. Conclusions: TRPV4 participated in the calcium oscillations and VSMC migration induced by PMVs. PMVs and the related molecules might be novel therapeutic targets for vascular remodeling during vascular injury. |
format | Online Article Text |
id | pubmed-7797689 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Ivyspring International Publisher |
record_format | MEDLINE/PubMed |
spelling | pubmed-77976892021-01-25 Platelet-derived microvesicles induce calcium oscillations and promote VSMC migration via TRPV4 Li, Shan-Shan Gao, Shuang Chen, Yi Bao, Han Li, Zi-Tong Yao, Qing-Ping Liu, Ji-Ting Wang, Yingxiao Qi, Ying-Xin Theranostics Research Paper Rationale: Abnormal migration of vascular smooth muscle cells (VSMCs) from the media to the interior is a critical process during the intimal restenosis caused by vascular injury. Here, we determined the role of platelet-derived microvesicles (PMVs) released by activated platelets in VSMC migration. Methods: A percutaneous transluminal angioplasty balloon dilatation catheter was used to establish vascular intimal injury. Collagen I was used to activate PMVs, mimicking collagen exposure during intimal injury. To determine the effects of PMVs on VSMC migration in vitro, scratch wound healing assays were performed. Fluorescence resonance energy transfer was used to detect variations of calcium dynamics in VSMCs. Results: Morphological results showed that neointimal hyperplasia was markedly increased after balloon injury of the carotid artery in rats, and the main component was VSMCs. PMVs significantly promoted single cell migration and wound closure in vitro. Fluorescence resonance energy transfer revealed that PMVs induced temporal and dynamic calcium oscillations in the cytoplasms of VSMCs. The influx of extracellular calcium, but not calcium from intracellular stores, was involved in the process described above. The channel antagonist GSK219 and specific siRNA revealed that a membrane calcium channel, transient receptor potential vanilloid 4 (TRPV4), participated in the calcium oscillations and VSMC migration induced by PMVs. Conclusions: TRPV4 participated in the calcium oscillations and VSMC migration induced by PMVs. PMVs and the related molecules might be novel therapeutic targets for vascular remodeling during vascular injury. Ivyspring International Publisher 2021-01-01 /pmc/articles/PMC7797689/ /pubmed/33500733 http://dx.doi.org/10.7150/thno.47182 Text en © The author(s) This is an open access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/). See http://ivyspring.com/terms for full terms and conditions. |
spellingShingle | Research Paper Li, Shan-Shan Gao, Shuang Chen, Yi Bao, Han Li, Zi-Tong Yao, Qing-Ping Liu, Ji-Ting Wang, Yingxiao Qi, Ying-Xin Platelet-derived microvesicles induce calcium oscillations and promote VSMC migration via TRPV4 |
title | Platelet-derived microvesicles induce calcium oscillations and promote VSMC migration via TRPV4 |
title_full | Platelet-derived microvesicles induce calcium oscillations and promote VSMC migration via TRPV4 |
title_fullStr | Platelet-derived microvesicles induce calcium oscillations and promote VSMC migration via TRPV4 |
title_full_unstemmed | Platelet-derived microvesicles induce calcium oscillations and promote VSMC migration via TRPV4 |
title_short | Platelet-derived microvesicles induce calcium oscillations and promote VSMC migration via TRPV4 |
title_sort | platelet-derived microvesicles induce calcium oscillations and promote vsmc migration via trpv4 |
topic | Research Paper |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7797689/ https://www.ncbi.nlm.nih.gov/pubmed/33500733 http://dx.doi.org/10.7150/thno.47182 |
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