title: The therapeutic potential of G-CSF in pressure overload induced ventricular reconstruction and heart failure in mice.
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.
authors: Department of Cardiology, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, 150 Jimo Road, Shanghai, 200120, China.
authors: Ji Ming
authors: JM
authors: Li
authors: Zhi Feng
authors: ZF
authors: Yao
authors: Yun Zeng
authors: YZ
authors: Zou
authors: Jun Bo
authors: JB
authors: Ge
authors: Ai Li
authors: AL
authors: Guan
authors: Jian
authors: J
authors: Wu
authors: Shou Ling
authors: SL
authors: Mi
authors: Yan Yan
authors: YY
authors: Liang
authors: Zhen
authors: Z
authors: Ma
mesh_terms: D000818:Animals; D001562:Benzimidazoles / Q000494:pharmacology / Q000627:therapeutic use; D001565:Benzoates / Q000494:pharmacology / Q000627:therapeutic use; D015153:Blotting, Western; D002339:Carotid Arteries / Q000601:surgery; D003250:Constriction; D017931:DNA Primers / Q000235:genetics; D004452:Echocardiography; D016179:Granulocyte Colony-Stimulating Factor / Q000494:pharmacology / Q000627:therapeutic use*; D006333:Heart Failure / Q000209:etiology* / Q000517:prevention & control*; D006973:Hypertension / Q000150:complications*; D017379:Hypertrophy, Left Ventricular / Q000150:complications / Q000188:drug therapy* / Q000209:etiology*; D051795:Hypoxia-Inducible Factor 1, alpha Subunit / Q000378:metabolism; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D008870:Microtubules / Q000473:pathology; D020133:Reverse Transcriptase Polymerase Chain Reaction; D000077333:Telmisartan; D042461:Vascular Endothelial Growth Factor A / Q000378:metabolism
chemical_list: D001562:Benzimidazoles; D001565:Benzoates; D017931:DNA Primers; C497443:Hif1a protein, mouse; D051795:Hypoxia-Inducible Factor 1, alpha Subunit; D042461:Vascular Endothelial Growth Factor A; D016179:Granulocyte Colony-Stimulating Factor; D000077333:Telmisartan