Attenuation of cardiac hypertrophy by G-CSF is associated with enhanced migration of bone marrow-derived cells.
Attenuation of cardiac hypertrophy by G-CSF is associated with enhanced migration of bone marrow-derived cells.
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DOI:
10.1111/jcmm.12494
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发表时间:
2015-05
影响因子:
5.3
通讯作者:
Brunner S
中科院分区:
文献类型:
--
作者:
Huber BC;Beetz NL;Laskowski A;Ziegler T;Grabmaier U;Kupatt C;Herbach N;Wanke R;Franz WM;Massberg S;Brunner S
Granulocyte-colony stimulating factor (G-CSF) has been shown to promote mobilization of bone marrow-derived stem cells (BMCs) into the bloodstream associated with improved survival and cardiac function after myocardial infarction. Therefore, the aim of the present study was to investigate whether G-CSF is able to attenuate cardiac remodelling in a mouse model of pressure-induced LV hypertrophy focusing on mobilization and migration of BMCs. LV hypertrophy was induced by transverse aortic constriction (TAC) in C57BL/6J mice. Four weeks after TAC procedure. Mice were treated with G-CSF (100 μg/kg/day; Amgen Biologicals) for 2 weeks. The number of migrated BMCs in the heart was analysed by flow cytometry. mRNA expression and protein level of different growth factors in the myocardium were investigated by RT-PCR and ELISA. Functional analyses assessed by echocardiography and immunohistochemical analysis were performed 8 weeks after TAC procedure. G-CSF-treated animals revealed enhanced homing of VLA-4+ and c-kit+ BMCs associated with increased mRNA expression and protein level of the corresponding homing factors Vascular cell adhesion protein 1 and Stem cell factor in the hypertrophic myocardium. Functionally, G-CSF significantly preserved LV function after TAC procedure, which was associated with a significantly reduced area of fibrosis compared to control animals. Furthermore, G-CSF-treated animals revealed a significant improvement of survival after TAC procedure. In summary, G-CSF treatment preserves cardiac function and is able to diminish cardiac fibrosis after induction of LV hypertrophy associated with increased homing of VLA-4+ and c-kit+ BMCs and enhanced expression of their respective homing factors VCAM-1 and SCF.
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影响因子:
5.3
作者:
Brunner S;Huber BC;Weinberger T;Vallaster M;Wollenweber T;Gerbitz A;Hacker M;Franz WM
通讯作者:
Franz WM
DOI:
10.1161/atvbaha.111.238618
发表时间:
2012-01
期刊:
Arteriosclerosis, thrombosis, and vascular biology
影响因子:
--
作者:
Sheikh AY;Huber BC;Narsinh KH;Spin JM;van der Bogt K;de Almeida PE;Ransohoff KJ;Kraft DL;Fajardo G;Ardigo D;Ransohoff J;Bernstein D;Fischbein MP;Robbins RC;Wu JC
通讯作者:
Wu JC
影响因子:
5.2
作者:
Huber, Bruno C.;Ransohoff, Julia D.;Ransohoff, Katherine J.;Riegler, Johannes;Ebert, Antje;Kodo, Kazuki;Gong, Yongquan;Sanchez-Freire, Veronica;Dey, Devaveena;Kooreman, Nigel G.;Diecke, Sebastian;Zhang, Wendy Y.;Odegaard, Justin;Hu, Shijun;Gold, Joseph D.;Robbins, Robert C.;Wu, Joseph C.
通讯作者:
Wu, Joseph C.
影响因子:
--
作者:
Baldo, Marcelo P.;Davel, Ana P. C.;Mill, Jose G.
通讯作者:
Mill, Jose G.
影响因子:
82.9
作者:
Kocher, AA;Schuster, MD;Itescu, S
通讯作者:
Itescu, S