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Updated: Oct 7, 2026
Acute Myocardial Infarction in Rats
Published on: February 16, 2011
A potential cardioprotective role of hepatocyte growth factor in myocardial infarction in rats
H Ueda1, T Nakamura, K Matsumoto
1Division of Biochemistry, Biomedical Research Center, Osaka University Graduate School of Medicine, Suita, Osaka 565-0871, Japan.
Insights
Hepatocyte growth factor (HGF) protects heart cells from death after myocardial infarction. The study found HGF levels and its receptor increase in infarcted rat hearts, suggesting a protective role for HGF in heart injury.
Area of Science:
- Cardiovascular Biology
- Regenerative Medicine
- Molecular Cardiology
Background:
- Cardiotrophic growth factors are explored for myocardial infarction treatment.
- Hepatocyte growth factor (HGF) is known for tissue repair but its role in the heart is unclear.
Purpose of the Study:
- To investigate the role of HGF in protecting the infarcted myocardium.
- To determine if HGF can protect cardiac myocytes from cell death.
Main Methods:
- Assessed c-Met/HGF receptor expression in cultured adult rat cardiac myocytes.
- Exposed cardiac myocytes to hydrogen peroxide and HGF to evaluate cell survival.
- Measured c-Met/HGF receptor and HGF mRNA levels in rat hearts before and after induced myocardial infarction.
- Used immunohistochemistry to localize c-Met receptor expression post-myocardial infarction.
Main Results:
- Cardiac myocytes express the c-Met/HGF receptor, which increases with cultivation.
- HGF treatment enhanced cardiac myocyte survival against oxidative stress induced by hydrogen peroxide.
- Myocardial infarction significantly increased c-Met/HGF receptor and HGF mRNA levels in rat hearts.
- The c-Met receptor was found in cardiomyocytes in border and non-infarcted regions after myocardial infarction.
Conclusions:
- The c-Met/HGF receptor is upregulated in cardiomyocytes following myocardial infarction.
- HGF demonstrates a protective effect on cardiac myocytes against oxidative stress.
- HGF may play a crucial role in myocardial protection after infarction.
Objective:
Cardiotrophic growth factors with anti-cell death actions on cardiac myocytes have gained attention for treatment of patients with myocardial infarction. Hepatocyte growth factor (HGF) plays a role in tissue repair and protection from injuries, however, the physiological role of HGF in the myocardium has not been well defined. We asked if HGF would afford to the infarcted myocardium.
Methods And Results:
Mature cardiac myocytes prepared from adult rats expressed barely detectable levels of the c-Met/HGF receptor, however, c-Met receptor expression increased during cultivation, which meant that cardiac myocytes are potential targets of HGF. Addition of hydrogen peroxide remarkably decreased the number of viable mature cardiac myocytes in primary culture, whereas treatment with HGF enhanced survival of the cells subjected to the oxidant stress. Although very low levels of c-Met/HGF receptor and HGF mRNA expression were seen in normal rat hearts, both c-Met/HGF receptor and HGF mRNA levels rapidly increased to much higher levels than normal, when the rats were subjected to myocardial infarction. Immunohistochemical analysis of the c-Met receptor indicated that this receptor was expressed in cardiomyocytes localized in the border regions of the viable myocardium and in non-infarcted regions following myocardial infarction.
Conclusion:
The c-Met/HGF receptor is induced in cardiomyocytes following myocardial infarction and HGF exhibits protective effect on cardiomyocytes against oxidative stress. Our working hypothesis is that HGF may afford myocardial protection from myocardial infarction.