Distinct Phenotypes Induced by Different Degrees of Transverse Aortic Constriction in C57BL/6N Mice

Haiyan Deng; Lei-Lei Ma; Fei-Juan Kong; Zengyong Qiao

doi:10.3389/fcvm.2021.641272

Distinct Phenotypes Induced by Different Degrees of Transverse Aortic Constriction in C57BL/6N Mice

Front Cardiovasc Med. 2021 Apr 22:8:641272. doi: 10.3389/fcvm.2021.641272. eCollection 2021.

Authors

Haiyan Deng¹, Lei-Lei Ma², Fei-Juan Kong^{3

4}, Zengyong Qiao¹

Affiliations

¹ Department of Cardiovascular Medicine, Shanghai Jiao Tong University Affiliated Sixth People's Hospital South Campus, Shanghai, China.
² Department of Cardiology, Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital, Fudan University, Shanghai, China.
³ Department of Endocrinology and Metabolism, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
⁴ Department of Endocrinology and Metabolism, Xuhui District Central Hospital of Shanghai, Shanghai, China.

Abstract

The transverse aortic constriction (TAC) model surgery is a widely used disease model to study pressure overload-induced cardiac hypertrophy and heart failure in mice. The severity of adverse cardiac remodeling of the TAC model is largely dependent on the degree of constriction around the aorta, and the phenotypes of TAC are also different in different mouse strains. Few studies focus on directly comparing phenotypes of the TAC model with different degrees of constriction around the aorta, and no study compares the difference in C57BL/6N mice. In the present study, C57BL/6N mice aged 10 weeks were subjected to sham, 25G TAC, 26G TAC, and 27G TAC surgery for 4 weeks. We then analyzed the different phenotypes induced by 25G TAC, 26G TAC, and 27G TAC in c57BL/6N mice in terms of pressure gradient, cardiac hypertrophy, cardiac function, heart failure situation, survival condition, and cardiac fibrosis. All C57BL/6N mice subjected to TAC surgery developed significantly hypertrophy. Mice subjected to 27G TAC had severe cardiac dysfunction, severe cardiac fibrosis, and exhibited characteristics of heart failure at 4 weeks post-TAC. Compared with 27G TAC mice, 26G TAC mice showed a much milder response in cardiac dysfunction and cardiac fibrosis compared to 27G TAC, and a very small fraction of the 26G TAC group exhibited characteristics of heart failure. There was no obvious cardiac dysfunction, cardiac fibrosis, and characteristics of heart failure observed in 25G TAC mice. Based on our results, we conclude that the 25G TAC, 26G TAC, and 27G TAC induced distinct phenotypes in C57BL/6N mice.

Keywords: C57BL/6N mice; cardiac fibrosis; cardiac hypertrophy; heart failure; transverse aortic constriction.