IL-27 promotes cardiac fibroblast activation and aggravates cardiac remodeling post myocardial infarction

Excessive and chronic inflammation post myocardial infarction (MI) causes cardiac fibrosis and progressive ventricular remodeling, which leads to heart failure. We previously found high levels of IL-27 in the heart and serum until day 14 in murine cardiac ischemia‒reperfusion injury models. However,...

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Main Authors: Xiaoxue Ma, Qingshu Meng, Shiyu Gong, Shanshan Shi, Xiaoting Liang, Fang Lin, Li Gong, Xuan Liu, Yinzhen Li, Mimi Li, Lu Wei, Wei Han, Leng Gao, Zhongmin Liu, Xiaohui Zhou
Format: Article
Language:English
Published: Elsevier 2023-06-01
Series:Heliyon
Subjects:
Online Access:http://www.sciencedirect.com/science/article/pii/S2405844023043074
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author Xiaoxue Ma
Qingshu Meng
Shiyu Gong
Shanshan Shi
Xiaoting Liang
Fang Lin
Li Gong
Xuan Liu
Yinzhen Li
Mimi Li
Lu Wei
Wei Han
Leng Gao
Zhongmin Liu
Xiaohui Zhou
author_facet Xiaoxue Ma
Qingshu Meng
Shiyu Gong
Shanshan Shi
Xiaoting Liang
Fang Lin
Li Gong
Xuan Liu
Yinzhen Li
Mimi Li
Lu Wei
Wei Han
Leng Gao
Zhongmin Liu
Xiaohui Zhou
author_sort Xiaoxue Ma
collection DOAJ
description Excessive and chronic inflammation post myocardial infarction (MI) causes cardiac fibrosis and progressive ventricular remodeling, which leads to heart failure. We previously found high levels of IL-27 in the heart and serum until day 14 in murine cardiac ischemia‒reperfusion injury models. However, whether IL-27 is involved in chronic inflammation-mediated ventricular remodeling remains unclear. In the present study, we found that MI triggered high IL-27 expression in murine cardiac macrophages. The increased expression of IL-27 in serum is correlated with cardiac dysfunction and aggravated fibrosis after MI. Furthermore, the addition of IL-27 significantly activated the JAK/STAT signaling pathway in cardiac fibroblasts (CFs). Meanwhile, IL-27 treatment promoted the proliferation, migration and extracellular matrix (ECM) production of CFs induced by angiotensin II (Ang II). Collectively, high levels of IL-27 mainly produced by cardiac macrophages post MI contribute to the activation of CFs and aggravate cardiac fibrosis.
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spelling doaj.art-ae431cb010404df29ee738634cc5db982023-06-22T05:04:22ZengElsevierHeliyon2405-84402023-06-0196e17099IL-27 promotes cardiac fibroblast activation and aggravates cardiac remodeling post myocardial infarctionXiaoxue Ma0Qingshu Meng1Shiyu Gong2Shanshan Shi3Xiaoting Liang4Fang Lin5Li Gong6Xuan Liu7Yinzhen Li8Mimi Li9Lu Wei10Wei Han11Leng Gao12Zhongmin Liu13Xiaohui Zhou14Shanghai East Hospital, Jinzhou Medical University, Jinzhou, 121000, China; Research Center for Translational Medicine, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, 200120, ChinaResearch Center for Translational Medicine, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, 200120, China; Shanghai Heart Failure Research Center, Shanghai, 200120, ChinaDepartment of Cardiology, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, 200120, ChinaResearch Center for Translational Medicine, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, 200120, China; Shanghai Heart Failure Research Center, Shanghai, 200120, ChinaResearch Center for Translational Medicine, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, 200120, ChinaResearch Center for Translational Medicine, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, 200120, China; Shanghai Heart Failure Research Center, Shanghai, 200120, ChinaShanghai East Hospital, Jinzhou Medical University, Jinzhou, 121000, China; Research Center for Translational Medicine, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, 200120, ChinaResearch Center for Translational Medicine, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, 200120, China; Department of Cardiovascular Surgery, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, 200120, ChinaResearch Center for Translational Medicine, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, 200120, ChinaResearch Center for Translational Medicine, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, 200120, China; Shanghai Heart Failure Research Center, Shanghai, 200120, ChinaResearch Center for Translational Medicine, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, 200120, China; Shanghai Heart Failure Research Center, Shanghai, 200120, ChinaDepartment of Heart Failure, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, 200120, ChinaTranslational Medical Center for Stem Cell Therapy & Institute for Regenerative Medicine, Shanghai East Hospital, Tongji University School of Medicine, Shanghai 200123, PR ChinaShanghai Heart Failure Research Center, Shanghai, 200120, China; Department of Cardiovascular Surgery, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, 200120, China; Shanghai Institute of Stem Cell Research and Clinical Translation, Shanghai 200120, China; Corresponding author. Research Center for Translational Medicine, Department of Cardiovascular Surgery, Shanghai East Hospital, Tongji University School of Medicine 150 Jimo Rd, Pudong, Shanghai, 200120, China.Research Center for Translational Medicine, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, 200120, China; Shanghai Heart Failure Research Center, Shanghai, 200120, China; Corresponding author. Research Center for Translational Medicine, Shanghai East Hospital, Tongji University School of Medicine 150 Jimo Rd, Pudong, Shanghai, 200120, ORCID, China.Excessive and chronic inflammation post myocardial infarction (MI) causes cardiac fibrosis and progressive ventricular remodeling, which leads to heart failure. We previously found high levels of IL-27 in the heart and serum until day 14 in murine cardiac ischemia‒reperfusion injury models. However, whether IL-27 is involved in chronic inflammation-mediated ventricular remodeling remains unclear. In the present study, we found that MI triggered high IL-27 expression in murine cardiac macrophages. The increased expression of IL-27 in serum is correlated with cardiac dysfunction and aggravated fibrosis after MI. Furthermore, the addition of IL-27 significantly activated the JAK/STAT signaling pathway in cardiac fibroblasts (CFs). Meanwhile, IL-27 treatment promoted the proliferation, migration and extracellular matrix (ECM) production of CFs induced by angiotensin II (Ang II). Collectively, high levels of IL-27 mainly produced by cardiac macrophages post MI contribute to the activation of CFs and aggravate cardiac fibrosis.http://www.sciencedirect.com/science/article/pii/S2405844023043074IL-27FibroblastMyocardial infarctionInflammationVentricular remodeling
spellingShingle Xiaoxue Ma
Qingshu Meng
Shiyu Gong
Shanshan Shi
Xiaoting Liang
Fang Lin
Li Gong
Xuan Liu
Yinzhen Li
Mimi Li
Lu Wei
Wei Han
Leng Gao
Zhongmin Liu
Xiaohui Zhou
IL-27 promotes cardiac fibroblast activation and aggravates cardiac remodeling post myocardial infarction
Heliyon
IL-27
Fibroblast
Myocardial infarction
Inflammation
Ventricular remodeling
title IL-27 promotes cardiac fibroblast activation and aggravates cardiac remodeling post myocardial infarction
title_full IL-27 promotes cardiac fibroblast activation and aggravates cardiac remodeling post myocardial infarction
title_fullStr IL-27 promotes cardiac fibroblast activation and aggravates cardiac remodeling post myocardial infarction
title_full_unstemmed IL-27 promotes cardiac fibroblast activation and aggravates cardiac remodeling post myocardial infarction
title_short IL-27 promotes cardiac fibroblast activation and aggravates cardiac remodeling post myocardial infarction
title_sort il 27 promotes cardiac fibroblast activation and aggravates cardiac remodeling post myocardial infarction
topic IL-27
Fibroblast
Myocardial infarction
Inflammation
Ventricular remodeling
url http://www.sciencedirect.com/science/article/pii/S2405844023043074
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