Effect of G-CSF on proangiogenic properties mobilized peripheral blood cells in patients with chronic heart failure
- Authors: Konenkov VI1, Poveshchenko OV1, Kim II1, Pokushalov EA2, Romanov AB2, Guleva NA1, Bernvald VV1, Shevchenko AV1, Golovanova OV1, Yankyate EV1, Poveshchenko AF1, Karaskov AM2
-
Affiliations:
- Research Institute of Clinical and Experimental Lymphology SB RAMS, Novosibirsk
- State Research Institute of Circulation Pathology them. Acad. EN Meshalkina, Novosibirsk
- Issue: Vol 6, No 3 (2011)
- Pages: 71-75
- Section: Articles
- URL: https://genescells.ru/2313-1829/article/view/121556
- DOI: https://doi.org/10.23868/gc121556
- ID: 121556
Cite item
Open Access
Access granted
Subscription or Fee Access
Abstract
cytokine-producing properties mobilized drug administration
G-CSF from bone marrow mononuclear cells of peripheral
blood of patients with heart failure, which developed after
acute myocardial infarction, in connection with the efficiency
of intramyocardial stem cell therapy. The study included 67
patients with CHD and III-IV functional class congestive
heart failure (NYHA), receiving current standard therapy.
Shown that the introduction of the drug G-CSF results in
mobilization of endothelial progenitor cells (EPC) from bone
marrow into peripheral blood (CD34+/CD133+and CD34+/
KDR+populations). Intramyocardial cell injection resulted in
improved perfusion at the injection site in 76% of patients.
Patients who responded to improved perfusion, the number of
CD34+CD133+PC in 3,2 times higher than in patients without
effect or impairment. Mononuclear cells after administration
of G-CSF in a 48 hour culture secrete cytokines, Epo,
GM-CSF, TNF-, contribute to the improvement of myocardial
perfusion. Peripheral blood is a readily available source of EPС,
and mononuclear cells after mobilization are able to exert
reparative effects on the ischemic myocardium.
About the authors
V I Konenkov
Research Institute of Clinical and Experimental Lymphology SB RAMS, NovosibirskResearch Institute of Clinical and Experimental Lymphology SB RAMS, Novosibirsk
O V Poveshchenko
Research Institute of Clinical and Experimental Lymphology SB RAMS, NovosibirskResearch Institute of Clinical and Experimental Lymphology SB RAMS, Novosibirsk
I I Kim
Research Institute of Clinical and Experimental Lymphology SB RAMS, NovosibirskResearch Institute of Clinical and Experimental Lymphology SB RAMS, Novosibirsk
E A Pokushalov
State Research Institute of Circulation Pathology them. Acad. EN Meshalkina, NovosibirskState Research Institute of Circulation Pathology them. Acad. EN Meshalkina, Novosibirsk
A B Romanov
State Research Institute of Circulation Pathology them. Acad. EN Meshalkina, NovosibirskState Research Institute of Circulation Pathology them. Acad. EN Meshalkina, Novosibirsk
N A Guleva
Research Institute of Clinical and Experimental Lymphology SB RAMS, NovosibirskResearch Institute of Clinical and Experimental Lymphology SB RAMS, Novosibirsk
V V Bernvald
Research Institute of Clinical and Experimental Lymphology SB RAMS, NovosibirskResearch Institute of Clinical and Experimental Lymphology SB RAMS, Novosibirsk
A V Shevchenko
Research Institute of Clinical and Experimental Lymphology SB RAMS, NovosibirskResearch Institute of Clinical and Experimental Lymphology SB RAMS, Novosibirsk
O V Golovanova
Research Institute of Clinical and Experimental Lymphology SB RAMS, NovosibirskResearch Institute of Clinical and Experimental Lymphology SB RAMS, Novosibirsk
E V Yankyate
Research Institute of Clinical and Experimental Lymphology SB RAMS, NovosibirskResearch Institute of Clinical and Experimental Lymphology SB RAMS, Novosibirsk
A F Poveshchenko
Research Institute of Clinical and Experimental Lymphology SB RAMS, NovosibirskResearch Institute of Clinical and Experimental Lymphology SB RAMS, Novosibirsk
A M Karaskov
State Research Institute of Circulation Pathology them. Acad. EN Meshalkina, NovosibirskState Research Institute of Circulation Pathology them. Acad. EN Meshalkina, Novosibirsk
References
- Harada M., Qin Y., Takano H. et al. G-CSF prevents cardiac remodeling after myocardial infarction by activating the Jak-Stat pathway in cardiomyocytes. Nat. Med. 2005; 11: 305-11.
- Wang Y., Tagil K., Ripa R.S. et al. Effect of mobilization of bone marrow stem cells by granulocyte colony stimulating factor on clinical symptoms, left ventricular perfusion and function in patients with severe chronic ischemic heart disease. Int. J. Cardiol. 2005; 100: 477-83.
- Asahara T., Murohara T., Sullivan A. et al. Isolation of putative progenitor endothelial cells for angiogenesis. Science 1997; 275: 964-7.
- Capobianco S., Chennamaneni V., Mittal M. et al. Endothelial progenitor cells as factors in neovascularization and endothelial repair. World J. Cardiol. 2010. 26; 2(12): 411-20
- de Boer H.C., Hovens M.M., van Oeveren-Rietdijk A.M. et al. Human CD34+/KDR+ cells are generated from circulating CD34+ cells after immobilization on activated platelets. Arterioscler. Thromb. Vasc. Biol. 2011; 31: 408-15.
- Dimmeler S., Leri A. Aging and disease as modifiers of efficacy of cell Therapy. Circ. Res. 2008; 102: 1319-30.
- Honold J., Lehmann R., Heeschen C. et al. Effects of granulocyte colony stimulating factor on functional activities of endothelial progenitor cells in patients with chronic ischemic heart disease. Arterioscler. Thromb. Vasc. Biol. 2006; 26: 2238-43.
- Leone A., Valgimigli M., Giannico M. B. et al. From bone marrow to the arterial wall: the ongoing tale of endothelial progenitor cells. European. Heart J. 2009; 30: 890-9.
- Zampetaki A., Kirton J., Xu Q. et.al. Vascular repair by endothelial progenitor cells. Cardiovascular. Research. 2008; 78: 413-21.
- Friedrich E.B., Walenta K., Scharlau J. et al. CD34-/CD133+/ VEGFR-2+ endothelial progenitor cell subpopulation with potent vasoregenerative capacities. Circ. Res. 2006; 98: e20-e25.
- Powell T.M., Paul J.D., Hill J.M. et al. Granulocyte colonystimulating factor mobilizes functional endothelial progenitor cells in patients with coronary artery disease. Arterioscler. Thromb. Vasc. Biol. 2005; 25: 296-301.
- Koyanagi M., Bushoven P., Iwasaki M. et al. Notch signaling contributes to the expression of cardiac markers in human circulating progenitor cells. Circ. Res. 2007; 101: 1139-45.
- Manginas A., Goussetis E., Koutelou M. et. al. Pilot study to evaluate the safety and feasibility of intracoronary CD133+ and CD133- CD34+ cell therapy in patients with nonviable anterior myocardial infarction. Catheter Cardiovasc. Interv. 2007; 69: 773-81.
- Tse H., Siu C., Zhu S. et al. Paracrine effects of direct intramyocardial implantation of bone marrow derived cells to enhance neovascularization in chronic ischaemic myocardium. Eur. J. Heart Fail. 2007; 9: 747-53.
- Martin-Rendon E., Brunskill S.J., Hyde C.J. et al. Autologous bone marrow stem cells to treat acute myocardial infarction: a systematic review. Eur. Heart J. 2008; 29: 1807-18.
- Arshed A.Т., Quyyumi E., Waller K.Т. et al. CD34+ cell infusion after ST elevation myocardial infarction is associated with improved perfusion and is dose dependent. Amer. Heart J. 2011; 161: 98-105.
- Gnecchi M., Zhang Z., Ni A. et al. Paracrine mechanisms in adult stem cell signaling and therapy. Circ. Res. 2008; 103: 1204-19.
- Latini R., Brines M., Fiordaliso F. Do non-hemopoietic effects of erythropoietin play a beneficial role in heart failure? Heart Fail. Rev. 2008; 13: 415-23.
- Dunlay S.M., Weston S.A., Redfield M.M. et al. Tumor necrosis factor-alpha and mortality in heart failure: a community study. Circulation 2008; 118: 625-31.
Supplementary files
