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Granulocyte colony-stimulating factor reduces cardiomyocyte apoptosis and improves cardiac function in
Xu Wei Hou1, Ja Son, Yang Wang
1State Key Laboratory of Experimental Hematology, Institute of Hematology, Chinese Academy of Medical Sciences and Peking Union Medical College, Tianjin, 30020, China.
Insights
Granulocyte colony-stimulating factor (G-CSF) treatment improved cardiac pump function and reduced cardiomyocyte apoptosis in a rat model of dilated cardiomyopathy (DCM). This study demonstrates G-CSF
Area of Science:
- Cardiology
- Molecular Biology
- Biomedical Research
Background:
- Cardiomyocyte apoptosis is implicated in dilated cardiomyopathy (DCM) progression.
- Granulocyte colony-stimulating factor (G-CSF) has shown potential in cardiac repair models.
- The effect of G-CSF on cardiac function and apoptosis in adriamycin-induced DCM was previously unstudied.
Purpose of the Study:
- To investigate the therapeutic potential of G-CSF in adriamycin (ADR)-induced DCM.
- To evaluate the impact of G-CSF on cardiac pump function and cardiomyocyte apoptosis.
- To assess G-CSF's effect on apoptosis-related protein Fas expression.
Main Methods:
- Wistar rats were induced with ADR and treated with G-CSF or placebo (PBS).
- Cardiac function was assessed using echocardiography and cardiac catheterization.
- Cardiomyocyte apoptosis was quantified using TUNEL assay, and Fas protein levels were measured by Western blot.
Main Results:
- ADR-induced DCM rats exhibited impaired cardiac function, elevated cardiomyocyte apoptosis, and high Fas expression.
- G-CSF treatment significantly improved left ventricular function compared to control groups.
- G-CSF administration markedly reduced cardiomyocyte apoptosis and Fas protein levels.
Conclusions:
- G-CSF administration effectively inhibits cardiomyocyte apoptosis and Fas protein expression in an ADR-induced DCM rat model.
- G-CSF treatment contributes to the improvement of cardiac pump function in vivo.
- G-CSF represents a potential therapeutic agent for DCM.
Background:
Cardiomyocyte apoptosis reportedly participates in the occurrence and progression of dilated cardiomyopathy (DCM). Recent studies have shown that granulocyte colony-stimulating factor (G-CSF) enhances bone marrow cells migration to the damaged heart in the DCM model and improves the ultrastructure of the cardiomyocyte in adriamycin (ADR) induced DCM. However, its influence on cardiac pump function and cardiomyocyte apoptosis has not been studied.
Methods And Materials:
Wistar Rats were randomly grouped into control, ADR, ADR+PBS, ADR+G-CSF group (n = 10). ADR (2.5 mg/kg, 6 times for 2 weeks) was administered intraperitoneally in all rats except the control group. After 2 weeks, the rats in ADR+G-CSF group were injected with G-CSF (50 microg/kg/day for 8 days) subcutaneously. Cardiac function was evaluated by echocardiogram and cardiac catheterization after 4 weeks. Cardiomyocytes apoptosis and apoptosis-related protein Fas were detected by in situ terminal deoxynucleotidyl transferase assay (TUNEL method) and Western blot, respectively.
Results:
The ADR and ADR+PBS groups showed significant deteriorations of left ventricular functions and high cardiomyocyte apoptosis index, as well as high Fas expressions. Meanwhile, the ADR+G-CSF group showed significant improvement in LV function, inhibition of cardiomyocyte apoptosis compared with the ADR and ADR+Phosphate-Buffered Saline PBS group. The Fas protein expression was remarkably attenuated as well.
Conclusion:
Our results suggest that administration of G-CSF inhibited cardiomyocyte apoptosis and Fas protein expression and contributes to improving cardiac pump function in vivo in ADR induced DCM rat model.
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