Granulocyte-CSF induced inflammation-associated cardiac thrombosis in iron loading mouse heart and can be attenuated by statin therapy View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2011-04-15

AUTHORS

Wei S Lian, Heng Lin, Winston TK Cheng, Tateki Kikuchi, Ching F Cheng

ABSTRACT

BACKGROUND: Granulocyte colony-stimulating factor (G-CSF), a hematopoietic cytokine, was recently used to treat patients of acute myocardial infarction with beneficial effect. However, controversy exists as some patients developed re-stenosis and worsened condition post G-CSF delivery. This study presents a new disease model to study G-CSF induced cardiac thrombosis and delineate its possible mechanism. We used iron loading to mimic condition of chronic cardiac dysfunction and apply G-CSF to mice to test our hypothesis. METHODS AND RESULTS: Eleven out of fifteen iron and G-CSF treated mice (I+G) showed thrombi formation in the left ventricular chamber with impaired cardiac function. Histological analysis revealed endothelial fibrosis, increased macrophage infiltration and tissue factor expression in the I+G mice hearts. Simvastatin treatment to I+G mice attenuated their cardiac apoptosis, iron deposition, and abrogated thrombus formation by attenuating systemic inflammation and leukocytosis, which was likely due to the activation of pAKT activation. However, thrombosis in I+G mice could not be suppressed by platelet receptor inhibitor, tirofiban. CONCLUSIONS: Our disease model demonstrated that G-CSF induces cardiac thrombosis through an inflammation-thrombosis interaction and this can be attenuated via statin therapy. Present study provides a mechanism and potential therapy for G-CSF induced cardiac thrombosis. More... »

PAGES

26-26

References to SciGraph publications

  • 1999-06. Regulation of endothelium-derived nitric oxide production by the protein kinase Akt in NATURE
  • 1999-06. Activation of nitric oxide synthase in endothelial cells by Akt-dependent phosphorylation in NATURE
  • 2006-01-17. Effects of G-CSF on left ventricular remodeling and heart failure after acute myocardial infarction in JOURNAL OF MOLECULAR MEDICINE
  • 2003-08-24. L-type Ca2+ channels provide a major pathway for iron entry into cardiomyocytes in iron-overload cardiomyopathy in NATURE MEDICINE
  • 2000-09. The HMG-CoA reductase inhibitor simvastatin activates the protein kinase Akt and promotes angiogenesis in normocholesterolemic animals. in NATURE MEDICINE
  • 2002-06-17. G-CSF induces stem cell mobilization by decreasing bone marrow SDF-1 and up-regulating CXCR4 in NATURE IMMUNOLOGY
  • 2005-02-20. G-CSF prevents cardiac remodeling after myocardial infarction by activating the Jak-Stat pathway in cardiomyocytes in NATURE MEDICINE
  • 2007-03-05. Granulocyte colony-stimulating factor improves left ventricular function of doxorubicin-induced cardiomyopathy in LABORATORY INVESTIGATION
  • 2007-01-22. Fetal alcohol exposure impairs hedgehog cholesterol modification and signaling in LABORATORY INVESTIGATION
  • 2003-02-18. Beyond lipid-lowering: effects of statins on endothelial nitric oxide in EUROPEAN JOURNAL OF CLINICAL PHARMACOLOGY
  • 2003-12-01. Administration of granulocyte-colony-stimulating factor for allogeneic hematopoietic cell collection may induce the tissue factor-dependent pathway in healthy donors in BONE MARROW TRANSPLANTATION
  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1186/1423-0127-18-26

    DOI

    http://dx.doi.org/10.1186/1423-0127-18-26

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1010768643

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/21496220


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