The therapeutic potential of G-CSF in pressure overload induced ventricular reconstruction and heart failure in mice
Autor: | Shou Ling Mi, Zhen Ma, Ji Ming Li, Ai Li Guan, Jun Bo Ge, Zhi Feng Yao, Yun Zeng Zou, Yan Yan Liang, Jian Wu |
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Rok vydání: | 2010 |
Předmět: |
Male
Vascular Endothelial Growth Factor A medicine.medical_specialty Myofilament Blotting Western Benzoates Microtubules Constriction Muscle hypertrophy Mice Internal medicine medicine.artery Ascending aorta Granulocyte Colony-Stimulating Factor Genetics medicine Animals Telmisartan Molecular Biology DNA Primers Pressure overload Heart Failure business.industry Reverse Transcriptase Polymerase Chain Reaction General Medicine medicine.disease Hypoxia-Inducible Factor 1 alpha Subunit Mice Inbred C57BL Carotid Arteries Echocardiography Heart failure Hypertension Cardiology Myocardial fibrosis Benzimidazoles Hypertrophy Left Ventricular business medicine.drug |
Zdroj: | Molecular biology reports. 39(1) |
ISSN: | 1573-4978 |
Popis: | In animal models of clinical entities causative of severe right and left ventricular (LV) pressure overload hypertrophy, increased density of the cellular microtubule network, through viscous loading of active myofilaments, causes contractile dysfunction that is normalized by microtubule depolymerization. In this study, 86 male mice were divided into seven groups. The transverse ascending aorta constriction (TAC) in six groups were performed in order to make heart failure model. Mice in each group were injected with G-CSF or/and telmisartan subcutaneously at different time respectively. Results showed that reduction in left ventricular volume and improved function persisted at 2 week, but recurrent dilatation at 4 weeks was associated with a loss of functional improvement. Compared with PBS group, the expression of VEGF protein and HIF-1 mRNA were significantly higher in mice injected with G-CSF or/and telmisartan (P < 0.05). The expression of p53 mRNA, myocardial fibrosis and mortality were significantly lower in mice injected with G-CSF or/and telmisartan (P < 0.05). It could be concluded that G-CSF can delay the progression of pressure overload induced ventricular reconstruction and heart failure in mice. |
Databáze: | OpenAIRE |
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