Are activated B cells involved in the process of myocardial fibrosis after acute myocardial infarction? An in vivo experiment
Abstract Background Inflammatory cells infiltrate into the ischemic and hypoxic myocardial tissue after myocardial infarction. B cells gather at the site of myocardial injury and secrete cytokines to regulate immune inflammation and fiber repair processes. Methods The animal experiment used ligation...
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BMC
2021-01-01
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Series: | BMC Cardiovascular Disorders |
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Online Access: | https://doi.org/10.1186/s12872-020-01775-9 |
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author | Fanrui Mo Ying Luo Yuluan Yan Juan Li Shayi Lai Weifeng Wu |
author_facet | Fanrui Mo Ying Luo Yuluan Yan Juan Li Shayi Lai Weifeng Wu |
author_sort | Fanrui Mo |
collection | DOAJ |
description | Abstract Background Inflammatory cells infiltrate into the ischemic and hypoxic myocardial tissue after myocardial infarction. B cells gather at the site of myocardial injury and secrete cytokines to regulate immune inflammation and fiber repair processes. Methods The animal experiment used ligation of the left anterior descending (LAD) artery of C57BL/6 mice to establish a mouse acute myocardial infarction (AMI) model to observe changes in activated B cells and cytokines at different time points. Twelve-week-old C57BL/6 male mice were randomly divided into the Sham group (24 mice) (thread under the LAD artery without ligation) and the AMI group (64 mice). In addition, C57BL/6 B-cell knockout (BKO) mice and C57BL/6 wild-type (WT) mice were used to establish AMI models to observe the expression levels of cardiomyocyte cytokines, such as TNF-α IL-1β, IL-6, TGF-β1, COL1-A1, COL3-AIII, TIMP, and MMP9. Moreover, pathological and collagen changes in the myocardium were analysed. One-way ANOVA and LSD method was used for comparisons of multiple and pairwise groups respectively. P < 0.05 indicated significant differences. Results An AMI model of C57BL/6 mice was established successfully. The ratio of activated B cells and the expression of TNF-α, IL-1β, IL-6, TGF-β1, and B cell activating factor (BAFF) in the 5-day subgroup were the highest in the myocardium, spleen and peripheral blood with the most obvious myocardial inflammatory cell infiltration. The cytokines mRNA expression levels in the 5-day subgroup of the BKO group were decreased compared with those in the WT group (P < 0.05). Among the 2-week subgroups of the Sham, WT and BKO groups, the the LVEDd and LVESd of the BKO group were lower than those of the WT group (P < 0.05), and the left ventricular ejection fraction was higher than that of the WT group (P < 0.05). Conclusion Activated B cells participate in the sustained state of myocardial inflammation and immune system activation after AMI, and may affect the metabolism of myocardial collagen after AMI by secreting cytokines. Moreover, B cells promote the expression of myocardial collagen Type I and Type III and damage the left ventricular ejection function. |
first_indexed | 2024-12-14T12:33:56Z |
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institution | Directory Open Access Journal |
issn | 1471-2261 |
language | English |
last_indexed | 2024-12-14T12:33:56Z |
publishDate | 2021-01-01 |
publisher | BMC |
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series | BMC Cardiovascular Disorders |
spelling | doaj.art-4e5dfad90e474327bfe16197d4a4885e2022-12-21T23:01:06ZengBMCBMC Cardiovascular Disorders1471-22612021-01-0121111410.1186/s12872-020-01775-9Are activated B cells involved in the process of myocardial fibrosis after acute myocardial infarction? An in vivo experimentFanrui Mo0Ying Luo1Yuluan Yan2Juan Li3Shayi Lai4Weifeng Wu5Department of Cardiology, The First Affiliated Hospital of Guangxi Medical UniversityGuangxi Medical UniversityDepartment of Cardiology, Fourth Affiliated Hospital of Guangxi Medical UniversityDepartment of Cardiology, Fourth Affiliated Hospital of Guangxi Medical UniversityDepartment of Cardiology, Fourth Affiliated Hospital of Guangxi Medical UniversityDepartment of Cardiology, The First Affiliated Hospital of Guangxi Medical UniversityAbstract Background Inflammatory cells infiltrate into the ischemic and hypoxic myocardial tissue after myocardial infarction. B cells gather at the site of myocardial injury and secrete cytokines to regulate immune inflammation and fiber repair processes. Methods The animal experiment used ligation of the left anterior descending (LAD) artery of C57BL/6 mice to establish a mouse acute myocardial infarction (AMI) model to observe changes in activated B cells and cytokines at different time points. Twelve-week-old C57BL/6 male mice were randomly divided into the Sham group (24 mice) (thread under the LAD artery without ligation) and the AMI group (64 mice). In addition, C57BL/6 B-cell knockout (BKO) mice and C57BL/6 wild-type (WT) mice were used to establish AMI models to observe the expression levels of cardiomyocyte cytokines, such as TNF-α IL-1β, IL-6, TGF-β1, COL1-A1, COL3-AIII, TIMP, and MMP9. Moreover, pathological and collagen changes in the myocardium were analysed. One-way ANOVA and LSD method was used for comparisons of multiple and pairwise groups respectively. P < 0.05 indicated significant differences. Results An AMI model of C57BL/6 mice was established successfully. The ratio of activated B cells and the expression of TNF-α, IL-1β, IL-6, TGF-β1, and B cell activating factor (BAFF) in the 5-day subgroup were the highest in the myocardium, spleen and peripheral blood with the most obvious myocardial inflammatory cell infiltration. The cytokines mRNA expression levels in the 5-day subgroup of the BKO group were decreased compared with those in the WT group (P < 0.05). Among the 2-week subgroups of the Sham, WT and BKO groups, the the LVEDd and LVESd of the BKO group were lower than those of the WT group (P < 0.05), and the left ventricular ejection fraction was higher than that of the WT group (P < 0.05). Conclusion Activated B cells participate in the sustained state of myocardial inflammation and immune system activation after AMI, and may affect the metabolism of myocardial collagen after AMI by secreting cytokines. Moreover, B cells promote the expression of myocardial collagen Type I and Type III and damage the left ventricular ejection function.https://doi.org/10.1186/s12872-020-01775-9Acute myocardial infarctionActivated B cellsCytokinesCollagenLeft ventricular function |
spellingShingle | Fanrui Mo Ying Luo Yuluan Yan Juan Li Shayi Lai Weifeng Wu Are activated B cells involved in the process of myocardial fibrosis after acute myocardial infarction? An in vivo experiment BMC Cardiovascular Disorders Acute myocardial infarction Activated B cells Cytokines Collagen Left ventricular function |
title | Are activated B cells involved in the process of myocardial fibrosis after acute myocardial infarction? An in vivo experiment |
title_full | Are activated B cells involved in the process of myocardial fibrosis after acute myocardial infarction? An in vivo experiment |
title_fullStr | Are activated B cells involved in the process of myocardial fibrosis after acute myocardial infarction? An in vivo experiment |
title_full_unstemmed | Are activated B cells involved in the process of myocardial fibrosis after acute myocardial infarction? An in vivo experiment |
title_short | Are activated B cells involved in the process of myocardial fibrosis after acute myocardial infarction? An in vivo experiment |
title_sort | are activated b cells involved in the process of myocardial fibrosis after acute myocardial infarction an in vivo experiment |
topic | Acute myocardial infarction Activated B cells Cytokines Collagen Left ventricular function |
url | https://doi.org/10.1186/s12872-020-01775-9 |
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