A Neonatal Mouse Model for Pressure Overload: Myocardial Response Corresponds to Severity

The heart regeneration after apical resection and myocardial infarction in neonatal mice has been studied for years. However, the response of neonatal mouse heart under pressure overload is seldom explored. This study aimed to induce pressure overload in neonatal mice through a transverse aortic con...

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Main Authors: Jielei Gu, Xuke Chen, Yangshuo Jin, Mingke Liu, Qiong Xu, Xiaolin Liu, Zhenyu Luo, Sisi Ling, Ningning Liu, Shiming Liu
Format: Article
Language:English
Published: Frontiers Media S.A. 2021-05-01
Series:Frontiers in Cardiovascular Medicine
Subjects:
Online Access:https://www.frontiersin.org/articles/10.3389/fcvm.2021.660246/full
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author Jielei Gu
Xuke Chen
Yangshuo Jin
Mingke Liu
Qiong Xu
Xiaolin Liu
Zhenyu Luo
Sisi Ling
Ningning Liu
Shiming Liu
author_facet Jielei Gu
Xuke Chen
Yangshuo Jin
Mingke Liu
Qiong Xu
Xiaolin Liu
Zhenyu Luo
Sisi Ling
Ningning Liu
Shiming Liu
author_sort Jielei Gu
collection DOAJ
description The heart regeneration after apical resection and myocardial infarction in neonatal mice has been studied for years. However, the response of neonatal mouse heart under pressure overload is seldom explored. This study aimed to induce pressure overload in neonatal mice through a transverse aortic constriction (TAC) with different-gauge needles so as to investigate the effect of pressure overload on cardiomyocyte proliferation and hypertrophy in these mice. Myocardial hypertrophy was evaluated by echocardiographic, pathological, and molecular analyses. Cardiomyocyte proliferation was detected by immune-staining of phospho-histone H3, Ki67, and 5-bromo-2-deoxyuridine. Mild pressure overload induced with a 30-gauge needle stimulated cardiomyocyte proliferation, adaptive hypertrophy, and angiogenesis. The heart function was not hampered even 21 days after the surgery. Moderate pressure overload induced with a 32-gauge needle led to pathological myocardial hypertrophy, fibrosis, and heart failure 7 days after the surgery. The gene and protein expression levels of markers of hypertrophy and fibrosis increased in 32-gauge TAC group compared with that in sham and 30-gauge TAC groups. The mice barely survived after severe pressure overload induced with a 34-gauge needle. The findings of this study might provide new insights into cardiomyocyte proliferation and hypertrophy in neonatal mice under pressure overload.
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spelling doaj.art-6902bff2f9f94f98860065fcf47f4df42022-12-21T18:28:45ZengFrontiers Media S.A.Frontiers in Cardiovascular Medicine2297-055X2021-05-01810.3389/fcvm.2021.660246660246A Neonatal Mouse Model for Pressure Overload: Myocardial Response Corresponds to SeverityJielei GuXuke ChenYangshuo JinMingke LiuQiong XuXiaolin LiuZhenyu LuoSisi LingNingning LiuShiming LiuThe heart regeneration after apical resection and myocardial infarction in neonatal mice has been studied for years. However, the response of neonatal mouse heart under pressure overload is seldom explored. This study aimed to induce pressure overload in neonatal mice through a transverse aortic constriction (TAC) with different-gauge needles so as to investigate the effect of pressure overload on cardiomyocyte proliferation and hypertrophy in these mice. Myocardial hypertrophy was evaluated by echocardiographic, pathological, and molecular analyses. Cardiomyocyte proliferation was detected by immune-staining of phospho-histone H3, Ki67, and 5-bromo-2-deoxyuridine. Mild pressure overload induced with a 30-gauge needle stimulated cardiomyocyte proliferation, adaptive hypertrophy, and angiogenesis. The heart function was not hampered even 21 days after the surgery. Moderate pressure overload induced with a 32-gauge needle led to pathological myocardial hypertrophy, fibrosis, and heart failure 7 days after the surgery. The gene and protein expression levels of markers of hypertrophy and fibrosis increased in 32-gauge TAC group compared with that in sham and 30-gauge TAC groups. The mice barely survived after severe pressure overload induced with a 34-gauge needle. The findings of this study might provide new insights into cardiomyocyte proliferation and hypertrophy in neonatal mice under pressure overload.https://www.frontiersin.org/articles/10.3389/fcvm.2021.660246/fullneonatal mousepressure overloadcardiomyocyte proliferationextracellular matrixmyocardial hypertrophy
spellingShingle Jielei Gu
Xuke Chen
Yangshuo Jin
Mingke Liu
Qiong Xu
Xiaolin Liu
Zhenyu Luo
Sisi Ling
Ningning Liu
Shiming Liu
A Neonatal Mouse Model for Pressure Overload: Myocardial Response Corresponds to Severity
Frontiers in Cardiovascular Medicine
neonatal mouse
pressure overload
cardiomyocyte proliferation
extracellular matrix
myocardial hypertrophy
title A Neonatal Mouse Model for Pressure Overload: Myocardial Response Corresponds to Severity
title_full A Neonatal Mouse Model for Pressure Overload: Myocardial Response Corresponds to Severity
title_fullStr A Neonatal Mouse Model for Pressure Overload: Myocardial Response Corresponds to Severity
title_full_unstemmed A Neonatal Mouse Model for Pressure Overload: Myocardial Response Corresponds to Severity
title_short A Neonatal Mouse Model for Pressure Overload: Myocardial Response Corresponds to Severity
title_sort neonatal mouse model for pressure overload myocardial response corresponds to severity
topic neonatal mouse
pressure overload
cardiomyocyte proliferation
extracellular matrix
myocardial hypertrophy
url https://www.frontiersin.org/articles/10.3389/fcvm.2021.660246/full
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