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Dronedarone hydrochloride enhances the bioactivity of endothelial progenitor cells via regulation of the AKT signaling pathway
Cardiovascular disease (CVD) and its complications are the leading cause of morbidity and mortality in the world. Because of the side effects and incomplete recovery from current therapy, stem cell therapy emerges as a potential therapy for CVD treatment, and endothelial progenitor cell (EPC) is one...
Autores principales: | , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
The Korean Physiological Society and The Korean Society of Pharmacology
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8405444/ https://www.ncbi.nlm.nih.gov/pubmed/34448463 http://dx.doi.org/10.4196/kjpp.2021.25.5.459 |
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author | Zhang, Jian Le, Thi Hong Van Rethineswaran, Vinoth Kumar Kim, Yeon-Ju Jang, Woong Bi Ji, Seung Taek Ly, Thanh Truong Giang Ha, Jong Seong Yun, Jisoo Cheong, Jae Hun Jung, Jinsup Kwon, Sang-Mo |
author_facet | Zhang, Jian Le, Thi Hong Van Rethineswaran, Vinoth Kumar Kim, Yeon-Ju Jang, Woong Bi Ji, Seung Taek Ly, Thanh Truong Giang Ha, Jong Seong Yun, Jisoo Cheong, Jae Hun Jung, Jinsup Kwon, Sang-Mo |
author_sort | Zhang, Jian |
collection | PubMed |
description | Cardiovascular disease (CVD) and its complications are the leading cause of morbidity and mortality in the world. Because of the side effects and incomplete recovery from current therapy, stem cell therapy emerges as a potential therapy for CVD treatment, and endothelial progenitor cell (EPC) is one of the key stem cells used for therapeutic applications. The effect of this therapy required the expansion of EPC function. To enhance the EPC activation, proliferation, and angiogenesis using dronedarone hydrochloride (DH) is the purpose of this study. DH received approval for atrial fibrillation treatment and its cardiovascular protective effects were already reported. In this study, DH significantly increased EPC proliferation, tube formation, migration, and maintained EPCs surface marker expression. In addition, DH treatment up-regulated the phosphorylation of AKT and reduced the reactive oxygen species production. In summary, the cell priming by DH considerably improved the functional activity of EPCs, and the use of which might be a novel strategy for CVD treatment. |
format | Online Article Text |
id | pubmed-8405444 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | The Korean Physiological Society and The Korean Society of Pharmacology |
record_format | MEDLINE/PubMed |
spelling | pubmed-84054442021-09-07 Dronedarone hydrochloride enhances the bioactivity of endothelial progenitor cells via regulation of the AKT signaling pathway Zhang, Jian Le, Thi Hong Van Rethineswaran, Vinoth Kumar Kim, Yeon-Ju Jang, Woong Bi Ji, Seung Taek Ly, Thanh Truong Giang Ha, Jong Seong Yun, Jisoo Cheong, Jae Hun Jung, Jinsup Kwon, Sang-Mo Korean J Physiol Pharmacol Original Article Cardiovascular disease (CVD) and its complications are the leading cause of morbidity and mortality in the world. Because of the side effects and incomplete recovery from current therapy, stem cell therapy emerges as a potential therapy for CVD treatment, and endothelial progenitor cell (EPC) is one of the key stem cells used for therapeutic applications. The effect of this therapy required the expansion of EPC function. To enhance the EPC activation, proliferation, and angiogenesis using dronedarone hydrochloride (DH) is the purpose of this study. DH received approval for atrial fibrillation treatment and its cardiovascular protective effects were already reported. In this study, DH significantly increased EPC proliferation, tube formation, migration, and maintained EPCs surface marker expression. In addition, DH treatment up-regulated the phosphorylation of AKT and reduced the reactive oxygen species production. In summary, the cell priming by DH considerably improved the functional activity of EPCs, and the use of which might be a novel strategy for CVD treatment. The Korean Physiological Society and The Korean Society of Pharmacology 2021-09-01 2021-09-01 /pmc/articles/PMC8405444/ /pubmed/34448463 http://dx.doi.org/10.4196/kjpp.2021.25.5.459 Text en Copyright © Korean J Physiol Pharmacol https://creativecommons.org/licenses/by-nc/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0 (https://creativecommons.org/licenses/by-nc/4.0/) ) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Article Zhang, Jian Le, Thi Hong Van Rethineswaran, Vinoth Kumar Kim, Yeon-Ju Jang, Woong Bi Ji, Seung Taek Ly, Thanh Truong Giang Ha, Jong Seong Yun, Jisoo Cheong, Jae Hun Jung, Jinsup Kwon, Sang-Mo Dronedarone hydrochloride enhances the bioactivity of endothelial progenitor cells via regulation of the AKT signaling pathway |
title | Dronedarone hydrochloride enhances the bioactivity of endothelial progenitor cells via regulation of the AKT signaling pathway |
title_full | Dronedarone hydrochloride enhances the bioactivity of endothelial progenitor cells via regulation of the AKT signaling pathway |
title_fullStr | Dronedarone hydrochloride enhances the bioactivity of endothelial progenitor cells via regulation of the AKT signaling pathway |
title_full_unstemmed | Dronedarone hydrochloride enhances the bioactivity of endothelial progenitor cells via regulation of the AKT signaling pathway |
title_short | Dronedarone hydrochloride enhances the bioactivity of endothelial progenitor cells via regulation of the AKT signaling pathway |
title_sort | dronedarone hydrochloride enhances the bioactivity of endothelial progenitor cells via regulation of the akt signaling pathway |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8405444/ https://www.ncbi.nlm.nih.gov/pubmed/34448463 http://dx.doi.org/10.4196/kjpp.2021.25.5.459 |
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