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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Format: | Article |
Language: | English |
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Wiley
2020-01-01
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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. |
format | Article |
id | doaj-art-d40e09d71408417f86ebaeffb3934b7b |
institution | Kabale University |
issn | 1755-5914 1755-5922 |
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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