Recombinant Human Brain Natriuretic Peptide Attenuates Myocardial Ischemia-Reperfusion Injury by Inhibiting CD4+ T Cell Proliferation via PI3K/AKT/mTOR Pathway Activation

Inflammation plays a major role in the development of myocardial ischemia-reperfusion (IR) injury. Recombinant human brain natriuretic peptide (rhBNP), a man-made version of a peptide that is elevated in heart failure, exhibits anti-inflammatory effects in various tissues. However, its role in myoca...

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Main Authors: Kun-Peng Li, Hai-Yan Zhang, Xiao-Dong Xu, Ming-Yang, Tie-Jun Li, Shu-Tian Song
Format: Article
Language:English
Published: Wiley 2020-01-01
Series:Cardiovascular Therapeutics
Online Access:http://dx.doi.org/10.1155/2020/1389312
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author Kun-Peng Li
Hai-Yan Zhang
Xiao-Dong Xu
Ming-Yang
Tie-Jun Li
Shu-Tian Song
author_facet Kun-Peng Li
Hai-Yan Zhang
Xiao-Dong Xu
Ming-Yang
Tie-Jun Li
Shu-Tian Song
author_sort Kun-Peng Li
collection DOAJ
description Inflammation plays a major role in the development of myocardial ischemia-reperfusion (IR) injury. Recombinant human brain natriuretic peptide (rhBNP), a man-made version of a peptide that is elevated in heart failure, exhibits anti-inflammatory effects in various tissues. However, its role in myocardial IR injury remains unclear. In this study, we demonstrate that treatment with rhBNP provided protection for mice against myocardial IR injury as manifested by reduced infarct size and well-preserved myocardial, attenuated inflammatory infiltration and CD4+ T cell proliferation function, and inhibited expression of proinflammatory related genes. Furthermore, mechanistic studies revealed that rhBNP inhibited Jurkat T proliferation by promoting PI3K/AKT/mTOR phosphorylation. Collectively, our data suggest that the administration of rhBNP during IR injury could expand our understanding of the cardioprotective effects of rhBNP.
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institution Kabale University
issn 1755-5914
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language English
publishDate 2020-01-01
publisher Wiley
record_format Article
series Cardiovascular Therapeutics
spelling doaj-art-d40e09d71408417f86ebaeffb3934b7b2025-02-03T01:00:07ZengWileyCardiovascular Therapeutics1755-59141755-59222020-01-01202010.1155/2020/13893121389312Recombinant Human Brain Natriuretic Peptide Attenuates Myocardial Ischemia-Reperfusion Injury by Inhibiting CD4+ T Cell Proliferation via PI3K/AKT/mTOR Pathway ActivationKun-Peng Li0Hai-Yan Zhang1Xiao-Dong Xu2Ming-Yang3Tie-Jun Li4Shu-Tian Song5Department of Cardiothoracic Surgery, The Cangzhou Central Hospital, Hebei Province 061001, ChinaDepartment of Nursing, Cangzhou Medical College, Hebei Province 061001, ChinaDepartment of Medicine, Cangzhou Medical College, Hebei Province 061001, ChinaDepartment of Cardiothoracic Surgery, The Cangzhou Central Hospital, Hebei Province 061001, ChinaDepartment of Anesthesiology, Cangzhou Central Hospital, Hebei Province 061001, ChinaDepartment of Cardiothoracic Surgery, The Cangzhou Central Hospital, Hebei Province 061001, ChinaInflammation plays a major role in the development of myocardial ischemia-reperfusion (IR) injury. Recombinant human brain natriuretic peptide (rhBNP), a man-made version of a peptide that is elevated in heart failure, exhibits anti-inflammatory effects in various tissues. However, its role in myocardial IR injury remains unclear. In this study, we demonstrate that treatment with rhBNP provided protection for mice against myocardial IR injury as manifested by reduced infarct size and well-preserved myocardial, attenuated inflammatory infiltration and CD4+ T cell proliferation function, and inhibited expression of proinflammatory related genes. Furthermore, mechanistic studies revealed that rhBNP inhibited Jurkat T proliferation by promoting PI3K/AKT/mTOR phosphorylation. Collectively, our data suggest that the administration of rhBNP during IR injury could expand our understanding of the cardioprotective effects of rhBNP.http://dx.doi.org/10.1155/2020/1389312
spellingShingle Kun-Peng Li
Hai-Yan Zhang
Xiao-Dong Xu
Ming-Yang
Tie-Jun Li
Shu-Tian Song
Recombinant Human Brain Natriuretic Peptide Attenuates Myocardial Ischemia-Reperfusion Injury by Inhibiting CD4+ T Cell Proliferation via PI3K/AKT/mTOR Pathway Activation
Cardiovascular Therapeutics
title Recombinant Human Brain Natriuretic Peptide Attenuates Myocardial Ischemia-Reperfusion Injury by Inhibiting CD4+ T Cell Proliferation via PI3K/AKT/mTOR Pathway Activation
title_full Recombinant Human Brain Natriuretic Peptide Attenuates Myocardial Ischemia-Reperfusion Injury by Inhibiting CD4+ T Cell Proliferation via PI3K/AKT/mTOR Pathway Activation
title_fullStr Recombinant Human Brain Natriuretic Peptide Attenuates Myocardial Ischemia-Reperfusion Injury by Inhibiting CD4+ T Cell Proliferation via PI3K/AKT/mTOR Pathway Activation
title_full_unstemmed Recombinant Human Brain Natriuretic Peptide Attenuates Myocardial Ischemia-Reperfusion Injury by Inhibiting CD4+ T Cell Proliferation via PI3K/AKT/mTOR Pathway Activation
title_short Recombinant Human Brain Natriuretic Peptide Attenuates Myocardial Ischemia-Reperfusion Injury by Inhibiting CD4+ T Cell Proliferation via PI3K/AKT/mTOR Pathway Activation
title_sort recombinant human brain natriuretic peptide attenuates myocardial ischemia reperfusion injury by inhibiting cd4 t cell proliferation via pi3k akt mtor pathway activation
url http://dx.doi.org/10.1155/2020/1389312
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