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- Titel:
Expression of CXCR4, VLA-1, LFA-3 and transducer of ERB in G-CSF-mobilised progenitor cells in acute myocardial infarction.
- Dokumenttyp:
- Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't; Article
- Autor(en):
- Stein, A; Zohlnhofer, D; Pogatsa-Murray, G; von Wedel, J; Steppich, BA; Schömig, A; Kastrati, A; Ott, I
- Abstract:
- G-CSF induced mobilisation of progenitor cells is a multistep processes involving chemokines, growth factors, matrix-degrading enzymes, and cell adhesive interactions mediated by specific receptors on haematopoietic cells. This study's aim was to investigate progenitor cells mobilised during myocardial infarction after treatment with granulocyte-stimulating factor (G-CSF). In the randomised, double-blind, placebo-controlled REVIVAL-2 study, 114 patients with acute myocardial infarction were included. Five days after successful percutaneous coronary intervention patients received either 10 microg/kg G-CSF (n=56) or placebo (n=58) subcutaneously for five days. Venous blood samples were analysed on day(s) 1, 3, 5 and 7 after therapy, and progenitor cell mobilisation and surface expression of VLA-4, LFA-1 and CXCR-4 was measured on circulating progenitor cells using flow cytometry. G-CSF induced a significant increase in circulating progenitor cells (72 +/- 20 cells/microl vs. 4.5 +/- 0.8 cells/microl, p<0.05). Surface expression of LFA-1, VLA-4 and CXCR4 on progenitor cells was decreased by 44%, 49% and 60% after G-CSF as compared to placebo (p<0.05). In accordance, mRNA expression of CXCR4 was reduced. Moreover, anti-proliferative transducer of ERB (TOB) mRNA was decreased, suggesting an increased proliferative potential of the mobilised progenitor cells. Decreased expression of adhesion and chemokine receptors on G-CSF mobilised progenitor cells in acute myocardial infarction may alter the homing capacity of circulating cells to the myocardium.
- Zeitschriftentitel:
- Thromb Haemost
- Jahr:
- 2010
- Band / Volume:
- 103
- Heft / Issue:
- 3
- Seitenangaben Beitrag:
- 638-43
- Sprache:
- eng
- Volltext / DOI:
- doi:10.1160/TH09-09-0657
- PubMed:
- http://view.ncbi.nlm.nih.gov/pubmed/20076856
- Print-ISSN:
- 0340-6245
- TUM Einrichtung:
- I. Medizinische Klinik und Poliklinik (Kardiologie)
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