Granulocyte-Colony Stimulating Factor Reduces Cardiomyocyte Apoptosis and Ameliorates Diastolic Dysfunction in Otsuka Long-Evans Tokushima Fatty Rats
- Authors
- Shin, Jeong Hun; Lim, Young-Hyo; Song, Yi-Sun; So, Byung-Im; Park, Jun-Young; Fang, Cheng-Hu; Lee, Yonggu; Kim, Hyuck; Kim, Kyung-Soo
- Issue Date
- 2014
- Publisher
- SPRINGER
- Keywords
- Apoptosis; Diabetic cardiomyopathy; G-CSF
- Citation
- CARDIOVASCULAR DRUGS AND THERAPY, v.28, no.3, pp.211 - 220
- Indexed
- SCIE
SCOPUS
- Journal Title
- CARDIOVASCULAR DRUGS AND THERAPY
- Volume
- 28
- Number
- 3
- Start Page
- 211
- End Page
- 220
- URI
- https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/161068
- DOI
- 10.1007/s10557-014-6519-8
- ISSN
- 0920-3206
- Abstract
- 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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