Downregulation of amphiregulin improves cardiac hypertrophy via attenuating oxidative stress and apoptosis
Abstract Amphiregulin (AREG) is a ligand of epidermal growth factor receptor and participates in the fibrosis of multiple organs. However, whether AREG can regulate hypertrophic cardiomyopathy is not well known. This research aims to explore the effect of AREG on cardiac hypertrophy, and whether the...
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BMC
2022-08-01
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Series: | Biology Direct |
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Online Access: | https://doi.org/10.1186/s13062-022-00334-w |
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author | Mingyue Ji Yun Liu Zhi Zuo Cheng Xu Li Lin Yong Li |
author_facet | Mingyue Ji Yun Liu Zhi Zuo Cheng Xu Li Lin Yong Li |
author_sort | Mingyue Ji |
collection | DOAJ |
description | Abstract Amphiregulin (AREG) is a ligand of epidermal growth factor receptor and participates in the fibrosis of multiple organs. However, whether AREG can regulate hypertrophic cardiomyopathy is not well known. This research aims to explore the effect of AREG on cardiac hypertrophy, and whether the oxidative stress and apoptosis was involved in the influence of AREG on cardiac hypertrophy. Angiotensin (Ang) II induced cardiac hypertrophy in mice and neonatal rat cardiomyocytes (NRCMs) or HL-1 cells in vitro. AREG expressions raised in the heart of mice. After AREG downregulation, the increases of Ang II induced cardiac weight and cardiomyocytes area were inhibited. Down-regulation of AREG could inhibit Ang II induced the increases of atrial natriuretic peptide, brain natriuretic peptide, beta-myosin heavy chain in the heart of mice, and NRCMs and HL-1 cells. The enhancement of oxidative stress in mice heart with Ang II treatment was alleviated by AREG knockdown. The raises of Ang II induced Bax and cleaved caspase3 in mice heart were inhibited by AREG downregulation. AREG downregulation reduced myocardial hypertrophy via inhibition of oxidative and apoptosis. AREG may be a target for future cardiac hypertrophy treatment. |
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issn | 1745-6150 |
language | English |
last_indexed | 2024-04-13T02:51:37Z |
publishDate | 2022-08-01 |
publisher | BMC |
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series | Biology Direct |
spelling | doaj.art-cb58fe147f8f44f0a7aabda61f7ad92e2022-12-22T03:05:49ZengBMCBiology Direct1745-61502022-08-0117111010.1186/s13062-022-00334-wDownregulation of amphiregulin improves cardiac hypertrophy via attenuating oxidative stress and apoptosisMingyue Ji0Yun Liu1Zhi Zuo2Cheng Xu3Li Lin4Yong Li5Department of Cardiology, Lianshui County People’s HospitalDepartment of Intensive Care Medicine, the First Affiliated Hospital of Nanjing Medical UniversityDepartment of Cardiology, the First Affiliated Hospital of Nanjing Medical UniversityDepartment of Cardiology, Lianshui County People’s HospitalDepartment of Cardiovascular Medicine, East Hospital, Tongji University School of MedicineDepartment of Cardiology, the First Affiliated Hospital of Nanjing Medical UniversityAbstract Amphiregulin (AREG) is a ligand of epidermal growth factor receptor and participates in the fibrosis of multiple organs. However, whether AREG can regulate hypertrophic cardiomyopathy is not well known. This research aims to explore the effect of AREG on cardiac hypertrophy, and whether the oxidative stress and apoptosis was involved in the influence of AREG on cardiac hypertrophy. Angiotensin (Ang) II induced cardiac hypertrophy in mice and neonatal rat cardiomyocytes (NRCMs) or HL-1 cells in vitro. AREG expressions raised in the heart of mice. After AREG downregulation, the increases of Ang II induced cardiac weight and cardiomyocytes area were inhibited. Down-regulation of AREG could inhibit Ang II induced the increases of atrial natriuretic peptide, brain natriuretic peptide, beta-myosin heavy chain in the heart of mice, and NRCMs and HL-1 cells. The enhancement of oxidative stress in mice heart with Ang II treatment was alleviated by AREG knockdown. The raises of Ang II induced Bax and cleaved caspase3 in mice heart were inhibited by AREG downregulation. AREG downregulation reduced myocardial hypertrophy via inhibition of oxidative and apoptosis. AREG may be a target for future cardiac hypertrophy treatment.https://doi.org/10.1186/s13062-022-00334-wAmphiregulinCardiac hypertrophyOxidative stressApoptosis |
spellingShingle | Mingyue Ji Yun Liu Zhi Zuo Cheng Xu Li Lin Yong Li Downregulation of amphiregulin improves cardiac hypertrophy via attenuating oxidative stress and apoptosis Biology Direct Amphiregulin Cardiac hypertrophy Oxidative stress Apoptosis |
title | Downregulation of amphiregulin improves cardiac hypertrophy via attenuating oxidative stress and apoptosis |
title_full | Downregulation of amphiregulin improves cardiac hypertrophy via attenuating oxidative stress and apoptosis |
title_fullStr | Downregulation of amphiregulin improves cardiac hypertrophy via attenuating oxidative stress and apoptosis |
title_full_unstemmed | Downregulation of amphiregulin improves cardiac hypertrophy via attenuating oxidative stress and apoptosis |
title_short | Downregulation of amphiregulin improves cardiac hypertrophy via attenuating oxidative stress and apoptosis |
title_sort | downregulation of amphiregulin improves cardiac hypertrophy via attenuating oxidative stress and apoptosis |
topic | Amphiregulin Cardiac hypertrophy Oxidative stress Apoptosis |
url | https://doi.org/10.1186/s13062-022-00334-w |
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