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Granulocyte-colony stimulating factor reduces cardiomyocyte apoptosis and ameliorates diastolic dysfunction in Otsuka
Jeong Hun Shin1, Young-Hyo Lim, Yi-Sun Song
1Cardiology division, Department of Internal Medicine, Hanyang University College of Medicine, 222 Wangsipri Street, Sungdong-gu, Seoul, 133-792, Republic of Korea.
Insights
Granulocyte-colony stimulating factor (G-CSF) improves cardiac function in diabetic cardiomyopathy by up-regulating G-CSF receptors and Bcl-2, reducing cardiomyocyte apoptosis. These findings highlight G-CSF's therapeutic potential for diabetic heart disease.
Area of Science:
- Cardiology
- Endocrinology
- Molecular Biology
Background:
- Granulocyte-colony stimulating factor (G-CSF) has demonstrated benefits in myocardial infarction and non-ischemic cardiomyopathies.
- The precise mechanisms by which G-CSF exerts beneficial effects in diabetic cardiomyopathy remain incompletely understood.
- Diabetic cardiomyopathy is a significant complication associated with type 2 diabetes.
Purpose of the Study:
- To investigate the underlying mechanisms of G-CSF action in a rat model of type 2 diabetic cardiomyopathy.
- To evaluate the impact of G-CSF on cardiac function, G-CSF receptor (GCSFR) expression, Bcl-2 levels, and cardiomyocyte apoptosis.
Main Methods:
- Seventeen-week-old Otsuka Long Evans Tokushima Fatty (OLETF) diabetic rats and Long Evans Tokushima Otsuka (LETO) rats were utilized.
- Rats were randomized to receive either G-CSF (100 μg/kg/day) or saline for 5 days.
- Cardiac function was assessed via serial echocardiography, and myocardial expression of GCSFR and Bcl-2, along with apoptosis, were measured.
Main Results:
- G-CSF treatment significantly improved cardiac diastolic function in diabetic rats.
- G-CSF administration led to the up-regulation of G-CSF receptor (GCSFR) expression in the diabetic myocardium.
- G-CSF treatment increased Bcl-2 expression and concurrently reduced cardiomyocyte apoptosis in diabetic hearts.
Conclusions:
- G-CSF demonstrates cardioprotective effects in diabetic cardiomyopathy, potentially via GCSFR up-regulation and apoptosis attenuation through Bcl-2.
- The observed glucose-lowering effect may also contribute to G-CSF's benefits.
- These findings support the exploration of G-CSF as a therapeutic agent for diabetic cardiomyopathy.
Background:
In recent studies, granulocyte-colony stimulating factor (G-CSF) was shown to improve cardiac function in myocardial infarction and non-ischemic cardiomyopathies. The mechanisms of these beneficial effects of G-CSF in diabetic cardiomyopathy are not yet fully understood. Therefore, we investigated the mechanisms of action of G-CSF on diabetic cardiomyopathy in a rat model of type 2 diabetes.
Methods:
Seventeen-week-old OLETF (Otsuka Long Evans Tokushima Fatty) diabetic rats and LETO (Long Evans Tokushima Otuska) rats were randomized to treatment with 5 days of G-CSF (100 μg/kg/day) or with saline. Cardiac function was evaluated by serial echocardiography performed before and 4 weeks after treatment. We measured expression of the G-CSF receptor (GCSFR) and Bcl-2, as well as the extent of apoptosis in the myocardium.
Results:
G-CSF treatment significantly improved cardiac diastolic function in the serial echocardiography assessments. Expression of G-CSFR was down-regulated in the diabetic myocardium (0.03 ± 0.12 % vs. 1 ± 0.15 %, p < 0.05), and its expression was stimulated by G-CSF treatment (0.03 ± 0.12 % vs. 0.42 ± 0.06 %, p < 0.05). In addition, G-CSF treatment increased the expression of Bcl-2 in the diabetic myocardium (0.69 ± 0.06 % vs. 0.26 ± 0.11 %, p < 0.05), consistent with the reduced cardiomyocyte apoptosis (9.38 ± 0.67 % vs. 17.28 ± 2.16 %, p < 0.05).
Conclusions:
Our results suggest that G-CSF might have a cardioprotective effect in diabetic cardiomyopathy through up-regulation of G-CSFR, attenuation of apoptosis by up-regulation of Bcl-2 expression, and glucose-lowering effect. Our findings support the therapeutic potential of G-CSF in diabetic cardiomyopathy.
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