The therapeutic potential of G-CSF in pressure overload induced ventricular reconstruction and heart failure in mice |
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Authors: | Ji Ming Li Zhi Feng Yao Yun Zeng Zou Jun Bo Ge Ai Li Guan Jian Wu Shou Ling Mi Yan Yan Liang Zhen Ma |
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Institution: | (1) Department of Cardiology, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, 150 Jimo Road, Shanghai, 200120, China;(2) Department of Cardiology, Zhongshan Hospital, Fudan University, Shanghai Institute of Cardiovascular Diseases, Shanghai, 200032, China;(3) Institutes of Biomedical Scienses, Fudan University, Shanghai, 200032, China; |
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Abstract: | 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. |
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