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Published on: August 30, 2022
Systemic heme oxygenase-1 transgenic overexpression aggravates pressure overload-induced cardiac hypertrophy in mice
Chang Chen1, Rong Huo, Yan Tong
1Department of Pharmacology, the State-Province Key Laboratories of Biomedicine-Pharmaceutics of China, Key Laboratory of Cardiovascular Research, Ministry of Education, Harbin Medical University, Harbin, PR China.
Insights
Systemic overexpression of heme oxygenase-1 (HO-1) worsened cardiac hypertrophy in mice subjected to pressure overload. This suggests HO-1 may not be protective in this model of cardiac hypertrophy.
Area of Science:
- Cardiovascular Biology
- Molecular Cardiology
- Genetic Engineering
Background:
- Heme oxygenase-1 (HO-1) has demonstrated protective effects against cardiac hypertrophy in various experimental models.
- Previous studies utilized HO-1 inducers, cardiac-specific transgenics, or animal treatments to explore its role.
Purpose of the Study:
- To investigate the impact of systemic HO-1 transgenic overexpression on pressure overload-induced cardiac hypertrophy in mice.
- To determine if systemic HO-1 overexpression exacerbates or ameliorates cardiac hypertrophy.
Main Methods:
- Cardiac hypertrophy was induced using transverse aortic constriction (TAC) in wild-type (WT) and systemic HO-1 transgenic (TG) mice.
- Evaluated parameters included heart and left ventricular weight/body weight indices, β-MHC protein expression, and cardiac interstitial fibrosis.
Main Results:
- Systemic HO-1 overexpression aggravated pressure overload-induced cardiac hypertrophy.
- TG mice showed increased heart/body weight, left ventricular/body weight, β-MHC expression, and fibrosis compared to WT mice post-TAC.
- While TAC increased HO-1 in WT, TG mice maintained higher HO-1 levels. Calcineurin expression was also elevated more in TG mice post-TAC.
Conclusions:
- Systemic HO-1 transgenic overexpression aggravates pressure overload-induced cardiac hypertrophy.
- This finding contrasts with previous studies and highlights a potential detrimental role of systemic HO-1 in this specific cardiac hypertrophy model.
Background/Aims:
Heme oxygenase-1(HO-1) has been reported to protect against cardiac hypertrophy in cultured neonatal cardiomyocytes treated with HO-1 inducer, cardiac specific HO-1 transgenic mice, or animals treated with HO-1 inducer. The aim of the present study is to examine the effects of systemic HO-1 transgenic overexpression on pressure overload-induced cardiac hypertrophy in mice.
Methods:
Pressure-overload cardiac hypertrophy was induced by transverse aortic constriction (TAC) in WT (wild type) and systemic HO-1 transgenic overexpression (TG) mice.
Results:
We found that systemic HO-1 transgenic overexpression aggravated pressure overload-induced cardiac hypertrophy. Pressure-overload induced the more increases of heart weight/ body weigh index, left ventricular weight/ body weight index, β-MHC protein expression, cardiac interstitial fibrosis in TG mice than in WT mice. Pressure-overload increased cardiac HO-1 protein expression in WT but not TG mice, but the cardiac HO-1 protein level was still higher in TAC-treated TG mice than in TAC-treated WT mice. The basal cardiac calcineurin protein level in TG mice was lower than that in WT mice. Pressure-overload increased calcineurin protein expression in both WT and TG mice; however, pressure-overload induced more calcineurin protein expression in TG mice than in WT mice.
Conclusion:
This study shows for the first time that systemic HO-1 transgenic overexpression aggravates pressure overload-induced cardiac hypertrophy.
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