IL-13 Derived Type 2 Innate Lymphocytes Ameliorates Cardiomyocyte Apoptosis Through STAT3 Signaling Pathway

IL-13 Derived Type 2 Innate Lymphocytes Ameliorates Cardiomyocyte Apoptosis Through STAT3 Signaling Pathway

The involvement of cardiomyopathy during sepsis means higher mortality and prolonged length of hospital stay. Many efforts have been made to alleviate the apoptosis of cardiomyocytes in sepsis. The huge potential of IL-13 in tissue repair has attracted increasing attention. In the present study, we...

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Main Authors: Ting Hong, Saiqi Li, Xiaoyu Guo, Yazhong Wei, Jingjing Zhang, Xiaohui Su, Miao Zhou, Haizhen Jin, Qing Miao, Lei Shen, Minfang Zhu, Bin He
Format: Article
Language:English
Published: Frontiers Media S.A. 2021-09-01
Series:Frontiers in Cell and Developmental Biology
Subjects:
sepsis
cardiomyocyte apoptosis
IL-13
ILC2
stat3
Online Access:https://www.frontiersin.org/articles/10.3389/fcell.2021.742662/full
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spelling doaj-f7d5f4e0546f49699c1f1a56d7c7c17c2021-09-20T05:23:07ZengFrontiers Media S.A.Frontiers in Cell and Developmental Biology2296-634X2021-09-01910.3389/fcell.2021.742662742662IL-13 Derived Type 2 Innate Lymphocytes Ameliorates Cardiomyocyte Apoptosis Through STAT3 Signaling PathwayTing Hong0Saiqi Li1Xiaoyu Guo2Yazhong Wei3Jingjing Zhang4Xiaohui Su5Miao Zhou6Haizhen Jin7Qing Miao8Lei Shen9Minfang Zhu10Bin He11Department of Critical Care Medicine, Shanghai Chest Hospital, Shanghai Jiao Tong University, Shanghai, ChinaDepartment of Critical Care Medicine, Shanghai Chest Hospital, Shanghai Jiao Tong University, Shanghai, ChinaDepartment of Critical Care Medicine, Shanghai Chest Hospital, Shanghai Jiao Tong University, Shanghai, ChinaDepartment of Critical Care Medicine, Shanghai Chest Hospital, Shanghai Jiao Tong University, Shanghai, ChinaShanghai Institute of Immunology, Shanghai Jiao Tong University School of Medicine, Shanghai, ChinaShanghai Institute of Immunology, Shanghai Jiao Tong University School of Medicine, Shanghai, ChinaDepartment of Anesthesiology and Surgical Intensive Care Unit, Xinhua Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, ChinaCentral Laboratory, Shanghai Chest Hospital, Shanghai Jiao Tong University, Shanghai, ChinaDepartments of Anesthesiology, Shanghai Chest Hospital, Shanghai Jiao Tong University, Shanghai, ChinaShanghai Institute of Immunology, Shanghai Jiao Tong University School of Medicine, Shanghai, ChinaDepartment of Critical Care Medicine, Shanghai Chest Hospital, Shanghai Jiao Tong University, Shanghai, ChinaDepartment of Critical Care Medicine, Shanghai Chest Hospital, Shanghai Jiao Tong University, Shanghai, ChinaThe involvement of cardiomyopathy during sepsis means higher mortality and prolonged length of hospital stay. Many efforts have been made to alleviate the apoptosis of cardiomyocytes in sepsis. The huge potential of IL-13 in tissue repair has attracted increasing attention. In the present study, we used LPS-treated mice or primary cardiomyocytes as a sepsis model to explore the anti-apoptotic ability of IL-13. It was found that an increased level of exogenous IL-13 was beneficial to the recovery of heart function in sepsis, and this anti-apoptotic effect of IL-13 was probably through enhancing the phosphorylation of STAT3 Ser727. In addition, we identified that the heart protective effect of IL-13 was associated with type 2 innate lymphocytes (ILC2). All these findings may provide a potential promising treatment for sepsis-induced cardiomyopathy.https://www.frontiersin.org/articles/10.3389/fcell.2021.742662/fullsepsiscardiomyocyte apoptosisIL-13ILC2stat3
collection DOAJ
language English
format Article
sources DOAJ
author Ting Hong
Saiqi Li
Xiaoyu Guo
Yazhong Wei
Jingjing Zhang
Xiaohui Su
Miao Zhou
Haizhen Jin
Qing Miao
Lei Shen
Minfang Zhu
Bin He
spellingShingle Ting Hong
Saiqi Li
Xiaoyu Guo
Yazhong Wei
Jingjing Zhang
Xiaohui Su
Miao Zhou
Haizhen Jin
Qing Miao
Lei Shen
Minfang Zhu
Bin He
IL-13 Derived Type 2 Innate Lymphocytes Ameliorates Cardiomyocyte Apoptosis Through STAT3 Signaling Pathway
Frontiers in Cell and Developmental Biology
sepsis
cardiomyocyte apoptosis
IL-13
ILC2
stat3
author_facet Ting Hong
Saiqi Li
Xiaoyu Guo
Yazhong Wei
Jingjing Zhang
Xiaohui Su
Miao Zhou
Haizhen Jin
Qing Miao
Lei Shen
Minfang Zhu
Bin He
author_sort Ting Hong
title IL-13 Derived Type 2 Innate Lymphocytes Ameliorates Cardiomyocyte Apoptosis Through STAT3 Signaling Pathway
title_short IL-13 Derived Type 2 Innate Lymphocytes Ameliorates Cardiomyocyte Apoptosis Through STAT3 Signaling Pathway
title_full IL-13 Derived Type 2 Innate Lymphocytes Ameliorates Cardiomyocyte Apoptosis Through STAT3 Signaling Pathway
title_fullStr IL-13 Derived Type 2 Innate Lymphocytes Ameliorates Cardiomyocyte Apoptosis Through STAT3 Signaling Pathway
title_full_unstemmed IL-13 Derived Type 2 Innate Lymphocytes Ameliorates Cardiomyocyte Apoptosis Through STAT3 Signaling Pathway
title_sort il-13 derived type 2 innate lymphocytes ameliorates cardiomyocyte apoptosis through stat3 signaling pathway
publisher Frontiers Media S.A.
series Frontiers in Cell and Developmental Biology
issn 2296-634X
publishDate 2021-09-01
description The involvement of cardiomyopathy during sepsis means higher mortality and prolonged length of hospital stay. Many efforts have been made to alleviate the apoptosis of cardiomyocytes in sepsis. The huge potential of IL-13 in tissue repair has attracted increasing attention. In the present study, we used LPS-treated mice or primary cardiomyocytes as a sepsis model to explore the anti-apoptotic ability of IL-13. It was found that an increased level of exogenous IL-13 was beneficial to the recovery of heart function in sepsis, and this anti-apoptotic effect of IL-13 was probably through enhancing the phosphorylation of STAT3 Ser727. In addition, we identified that the heart protective effect of IL-13 was associated with type 2 innate lymphocytes (ILC2). All these findings may provide a potential promising treatment for sepsis-induced cardiomyopathy.
topic sepsis
cardiomyocyte apoptosis
IL-13
ILC2
stat3
url https://www.frontiersin.org/articles/10.3389/fcell.2021.742662/full
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