PRDX2 in Myocyte Hypertrophy and Survival is Mediated by TLR4 in Acute Infarcted Myocardium

Abstract Peroxiredoxin 2 (PRDX2) is an antioxidant and molecular chaperone that can be secreted from tumor cells. But the role of PRDX2 in acute myocardial infarction (AMI) is not clear. In the current study, we demonstrate the role of PRDX2 from clinical trials, H9c2 cells and in a mouse model. ELI...

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Autores principales:	Xian Jin, Chengjun Chen, Dandan Li, Qian Su, Yanwen Hang, Peng Zhang, Wei Hu
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2017
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/22e81565c2e0410a81ee9c2d38113ec1
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spelling	oai:doaj.org-article:22e81565c2e0410a81ee9c2d38113ec12021-12-02T16:06:37ZPRDX2 in Myocyte Hypertrophy and Survival is Mediated by TLR4 in Acute Infarcted Myocardium10.1038/s41598-017-06718-72045-2322https://doaj.org/article/22e81565c2e0410a81ee9c2d38113ec12017-08-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-06718-7https://doaj.org/toc/2045-2322Abstract Peroxiredoxin 2 (PRDX2) is an antioxidant and molecular chaperone that can be secreted from tumor cells. But the role of PRDX2 in acute myocardial infarction (AMI) is not clear. In the current study, we demonstrate the role of PRDX2 from clinical trials, H9c2 cells and in a mouse model. ELISA analysis shows that serum concentrations of VEGF and inflammatory factor IL-1β, TNF-α and IL-6 were increased in AMI patients compared to a control group. The expression of PRDX2 was also upregulated. In vivo experiments show that the expression of PRDX2 inhibits hypoxia-induced oxidative stress injury to H9c2 cells. However, PRDX2 expression promotes TLR4 mediated inflammatory factor expression and VEGF expression under hypoxia conditions. PRDX2 overexpression in H9c2 cells also promotes human endothelial cell migration, vasculogenic mimicry formation and myocardial hypertrophy related protein expression. The overexpression of PRDX2 inhibits ROS level and myocardial injury after AMI but promotes inflammatory responses in vivo. Immunocytochemistry and immunofluorescence analysis show that overexpression of PRDX2 promotes angiogenesis and myocardial hypertrophy. Taken together, our results indicate that PRDX2 plays two roles in acute infarction – the promotion of cell survival and inflammatory myocardial hypertrophy.Xian JinChengjun ChenDandan LiQian SuYanwen HangPeng ZhangWei HuNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-13 (2017)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Xian Jin Chengjun Chen Dandan Li Qian Su Yanwen Hang Peng Zhang Wei Hu PRDX2 in Myocyte Hypertrophy and Survival is Mediated by TLR4 in Acute Infarcted Myocardium
description	Abstract Peroxiredoxin 2 (PRDX2) is an antioxidant and molecular chaperone that can be secreted from tumor cells. But the role of PRDX2 in acute myocardial infarction (AMI) is not clear. In the current study, we demonstrate the role of PRDX2 from clinical trials, H9c2 cells and in a mouse model. ELISA analysis shows that serum concentrations of VEGF and inflammatory factor IL-1β, TNF-α and IL-6 were increased in AMI patients compared to a control group. The expression of PRDX2 was also upregulated. In vivo experiments show that the expression of PRDX2 inhibits hypoxia-induced oxidative stress injury to H9c2 cells. However, PRDX2 expression promotes TLR4 mediated inflammatory factor expression and VEGF expression under hypoxia conditions. PRDX2 overexpression in H9c2 cells also promotes human endothelial cell migration, vasculogenic mimicry formation and myocardial hypertrophy related protein expression. The overexpression of PRDX2 inhibits ROS level and myocardial injury after AMI but promotes inflammatory responses in vivo. Immunocytochemistry and immunofluorescence analysis show that overexpression of PRDX2 promotes angiogenesis and myocardial hypertrophy. Taken together, our results indicate that PRDX2 plays two roles in acute infarction – the promotion of cell survival and inflammatory myocardial hypertrophy.
format	article
author	Xian Jin Chengjun Chen Dandan Li Qian Su Yanwen Hang Peng Zhang Wei Hu
author_facet	Xian Jin Chengjun Chen Dandan Li Qian Su Yanwen Hang Peng Zhang Wei Hu
author_sort	Xian Jin
title	PRDX2 in Myocyte Hypertrophy and Survival is Mediated by TLR4 in Acute Infarcted Myocardium
title_short	PRDX2 in Myocyte Hypertrophy and Survival is Mediated by TLR4 in Acute Infarcted Myocardium
title_full	PRDX2 in Myocyte Hypertrophy and Survival is Mediated by TLR4 in Acute Infarcted Myocardium
title_fullStr	PRDX2 in Myocyte Hypertrophy and Survival is Mediated by TLR4 in Acute Infarcted Myocardium
title_full_unstemmed	PRDX2 in Myocyte Hypertrophy and Survival is Mediated by TLR4 in Acute Infarcted Myocardium
title_sort	prdx2 in myocyte hypertrophy and survival is mediated by tlr4 in acute infarcted myocardium
publisher	Nature Portfolio
publishDate	2017
url	https://doaj.org/article/22e81565c2e0410a81ee9c2d38113ec1
work_keys_str_mv	AT xianjin prdx2inmyocytehypertrophyandsurvivalismediatedbytlr4inacuteinfarctedmyocardium AT chengjunchen prdx2inmyocytehypertrophyandsurvivalismediatedbytlr4inacuteinfarctedmyocardium AT dandanli prdx2inmyocytehypertrophyandsurvivalismediatedbytlr4inacuteinfarctedmyocardium AT qiansu prdx2inmyocytehypertrophyandsurvivalismediatedbytlr4inacuteinfarctedmyocardium AT yanwenhang prdx2inmyocytehypertrophyandsurvivalismediatedbytlr4inacuteinfarctedmyocardium AT pengzhang prdx2inmyocytehypertrophyandsurvivalismediatedbytlr4inacuteinfarctedmyocardium AT weihu prdx2inmyocytehypertrophyandsurvivalismediatedbytlr4inacuteinfarctedmyocardium
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PRDX2 in Myocyte Hypertrophy and Survival is Mediated by TLR4 in Acute Infarcted Myocardium

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