IL-27 promotes cardiac fibroblast activation and aggravates cardiac remodeling post myocardial infarction
© 2023 The Authors..
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.
| Medienart: |
E-Artikel |
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| Erscheinungsjahr: |
2023 |
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| Erschienen: |
2023 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:9 |
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| Enthalten in: |
Heliyon - 9(2023), 6 vom: 29. Juni, Seite e17099 |
| Sprache: |
Englisch |
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| Beteiligte Personen: |
Ma, Xiaoxue [VerfasserIn] |
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| Links: |
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| Themen: |
Fibroblast |
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| Anmerkungen: |
Date Revised 18.07.2023 published: Electronic-eCollection Citation Status PubMed-not-MEDLINE |
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| doi: |
10.1016/j.heliyon.2023.e17099 |
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| funding: |
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| Förderinstitution / Projekttitel: |
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| PPN (Katalog-ID): |
NLM35942175X |
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| 520 | |a © 2023 The Authors. | ||
| 520 | |a 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 | ||
| 650 | 4 | |a Journal Article | |
| 650 | 4 | |a Fibroblast | |
| 650 | 4 | |a IL-27 | |
| 650 | 4 | |a Inflammation | |
| 650 | 4 | |a Myocardial infarction | |
| 650 | 4 | |a Ventricular remodeling | |
| 700 | 1 | |a Meng, Qingshu |e verfasserin |4 aut | |
| 700 | 1 | |a Gong, Shiyu |e verfasserin |4 aut | |
| 700 | 1 | |a Shi, Shanshan |e verfasserin |4 aut | |
| 700 | 1 | |a Liang, Xiaoting |e verfasserin |4 aut | |
| 700 | 1 | |a Lin, Fang |e verfasserin |4 aut | |
| 700 | 1 | |a Gong, Li |e verfasserin |4 aut | |
| 700 | 1 | |a Liu, Xuan |e verfasserin |4 aut | |
| 700 | 1 | |a Li, Yinzhen |e verfasserin |4 aut | |
| 700 | 1 | |a Li, Mimi |e verfasserin |4 aut | |
| 700 | 1 | |a Wei, Lu |e verfasserin |4 aut | |
| 700 | 1 | |a Han, Wei |e verfasserin |4 aut | |
| 700 | 1 | |a Gao, Leng |e verfasserin |4 aut | |
| 700 | 1 | |a Liu, Zhongmin |e verfasserin |4 aut | |
| 700 | 1 | |a Zhou, Xiaohui |e verfasserin |4 aut | |
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