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Dental pulp-derived stem cell conditioned medium reduces cardiac injury following ischemia-reperfusion

Stem cells from human exfoliated deciduous teeth (SHEDs) can regenerate various tissues. We investigated the impact of SHED-conditioned medium (SHED-CM) on myocardial injury in a mouse model of ischemia-reperfusion (I/R). Wild-type (WT) mice were subjected to myocardial ischemia followed by reperfus...

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Autores principales: Yamaguchi, Satoshi, Shibata, Rei, Yamamoto, Noriyuki, Nishikawa, Masaya, Hibi, Hideharu, Tanigawa, Tohru, Ueda, Minoru, Murohara, Toyoaki, Yamamoto, Akihito
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4635346/
https://www.ncbi.nlm.nih.gov/pubmed/26542315
http://dx.doi.org/10.1038/srep16295
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author Yamaguchi, Satoshi
Shibata, Rei
Yamamoto, Noriyuki
Nishikawa, Masaya
Hibi, Hideharu
Tanigawa, Tohru
Ueda, Minoru
Murohara, Toyoaki
Yamamoto, Akihito
author_facet Yamaguchi, Satoshi
Shibata, Rei
Yamamoto, Noriyuki
Nishikawa, Masaya
Hibi, Hideharu
Tanigawa, Tohru
Ueda, Minoru
Murohara, Toyoaki
Yamamoto, Akihito
author_sort Yamaguchi, Satoshi
collection PubMed
description Stem cells from human exfoliated deciduous teeth (SHEDs) can regenerate various tissues. We investigated the impact of SHED-conditioned medium (SHED-CM) on myocardial injury in a mouse model of ischemia-reperfusion (I/R). Wild-type (WT) mice were subjected to myocardial ischemia followed by reperfusion. SHED-CM was intravenously injected at 5 min after reperfusion. Administration of SHED-CM reduced myocardial infarct size as well as decreased apoptosis and inflammatory cytokine levels, such as TNF-α, IL-6, and IL-β, in the myocardium following I/R. In cultured cardiac myocytes, SHED-CM significantly suppressed apoptosis under hypoxia/serum-deprivation and reduced LPS-induced expression of pro-inflammatory genes. Furthermore, anti-apoptotic action of SHED-CM was stronger than bone marrow-derived stem cell (BMSC)-CM or adipose-derived stem cell (ADSC)-CM in cardiac myocytes. SHED-CM contains a higher concentration of hepatocyte growth factor (HGF) than BMSC-CM and ADSC-CM, and neutralization of HGF attenuated the inhibitory actions of SHED-CM on apoptosis in cardiac myocytes. Finally, WT mice were intravenously treated with an HGF-depleted SHED-CM, followed by myocardial I/R. HGF depletion significantly attenuated the inhibitory actions of SHED-CM on myocardial infarct size and apoptosis after I/R. SHED-CM protects the heart from acute ischemic injury because it suppresses inflammation and apoptosis. SHED-CM could be a useful treatment option for acute myocardial infarction.
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spelling pubmed-46353462015-11-25 Dental pulp-derived stem cell conditioned medium reduces cardiac injury following ischemia-reperfusion Yamaguchi, Satoshi Shibata, Rei Yamamoto, Noriyuki Nishikawa, Masaya Hibi, Hideharu Tanigawa, Tohru Ueda, Minoru Murohara, Toyoaki Yamamoto, Akihito Sci Rep Article Stem cells from human exfoliated deciduous teeth (SHEDs) can regenerate various tissues. We investigated the impact of SHED-conditioned medium (SHED-CM) on myocardial injury in a mouse model of ischemia-reperfusion (I/R). Wild-type (WT) mice were subjected to myocardial ischemia followed by reperfusion. SHED-CM was intravenously injected at 5 min after reperfusion. Administration of SHED-CM reduced myocardial infarct size as well as decreased apoptosis and inflammatory cytokine levels, such as TNF-α, IL-6, and IL-β, in the myocardium following I/R. In cultured cardiac myocytes, SHED-CM significantly suppressed apoptosis under hypoxia/serum-deprivation and reduced LPS-induced expression of pro-inflammatory genes. Furthermore, anti-apoptotic action of SHED-CM was stronger than bone marrow-derived stem cell (BMSC)-CM or adipose-derived stem cell (ADSC)-CM in cardiac myocytes. SHED-CM contains a higher concentration of hepatocyte growth factor (HGF) than BMSC-CM and ADSC-CM, and neutralization of HGF attenuated the inhibitory actions of SHED-CM on apoptosis in cardiac myocytes. Finally, WT mice were intravenously treated with an HGF-depleted SHED-CM, followed by myocardial I/R. HGF depletion significantly attenuated the inhibitory actions of SHED-CM on myocardial infarct size and apoptosis after I/R. SHED-CM protects the heart from acute ischemic injury because it suppresses inflammation and apoptosis. SHED-CM could be a useful treatment option for acute myocardial infarction. Nature Publishing Group 2015-11-06 /pmc/articles/PMC4635346/ /pubmed/26542315 http://dx.doi.org/10.1038/srep16295 Text en Copyright © 2015, Macmillan Publishers Limited http://creativecommons.org/licenses/by/4.0/ 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/
spellingShingle Article
Yamaguchi, Satoshi
Shibata, Rei
Yamamoto, Noriyuki
Nishikawa, Masaya
Hibi, Hideharu
Tanigawa, Tohru
Ueda, Minoru
Murohara, Toyoaki
Yamamoto, Akihito
Dental pulp-derived stem cell conditioned medium reduces cardiac injury following ischemia-reperfusion
title Dental pulp-derived stem cell conditioned medium reduces cardiac injury following ischemia-reperfusion
title_full Dental pulp-derived stem cell conditioned medium reduces cardiac injury following ischemia-reperfusion
title_fullStr Dental pulp-derived stem cell conditioned medium reduces cardiac injury following ischemia-reperfusion
title_full_unstemmed Dental pulp-derived stem cell conditioned medium reduces cardiac injury following ischemia-reperfusion
title_short Dental pulp-derived stem cell conditioned medium reduces cardiac injury following ischemia-reperfusion
title_sort dental pulp-derived stem cell conditioned medium reduces cardiac injury following ischemia-reperfusion
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4635346/
https://www.ncbi.nlm.nih.gov/pubmed/26542315
http://dx.doi.org/10.1038/srep16295
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