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Granulocyte colony-stimulating factor and stem cell factor improve endogenous repair after myocardial infarction.
Cardiovasc Res. 2006 Apr 01; 70(1):117-25.CR

Abstract

OBJECTIVE

The aims of this study were, first, to determine if granulocyte colony-stimulating factor (G-CSF) and stem cell factor (SCF) improved left ventricular function in the setting of a reperfusion model of myocardial infarction (MI) and, second, to evaluate the effects of G-CSF/SCF on cellular repair and, in particular, the fate of bone marrow cells homing to the site of tissue injury.

METHODS

MI was induced in mice by transient ligation of the left descending coronary artery. G-CSF/SCF were administered for 5 days after MI. Cardiac function was assessed 28 days after MI. The effect of G-CSF/SCF on the cellular composition of the infarct region was assessed by immunohistochemistry. MI was performed in mice reconstituted with bone marrow cells expressing DsRed to track the fate of bone marrow-derived cells within the infarct region.

RESULTS

G-CSF/SCF-treated mice had significantly improved left ventricular (LV) function as determined by LV developed pressure, LV+/-dp/dt(max/min), and LV end-diastolic pressure. G-CSF alone produced similar improvements in cardiac function. These improvements in LV function were associated with 70% more blood vessels and a doubling of cells expressing cardiomyocyte-specific transcription factors GATA-4, Nkx2.5 and alpha-actinin cells within the infarct zone. Cells within the infarct expressing stromal-derived factor also increased by 200%. To elucidate the origin of these cells, bone marrow chimeras, where hematopoietic cells expressed the fluorescent marker DsRed, were treated with G-CSF/SCF after MI. Bone marrow-derived, DsRed-expressing cells in the infarct region of G-CSF/SCF-treated chimeras increased by an average of 12-fold; however, the vast majority of DsRed cells expressed the hematopoietic-specific marker CD45 but not blood vessel or cardiomyocyte markers.

CONCLUSIONS

G-CSF/SCF therapy improved cardiac function when delivered after MI, increasing the number of blood vessels and cells of cardiomyogenic lineage. However, these cells were of myocardial rather than bone marrow origin.

Authors+Show Affiliations

Cell Biology Laboratory, Baker Heart Research Institute, Melbourne, Australia.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

16497284

Citation

Kanellakis, Peter, et al. "Granulocyte Colony-stimulating Factor and Stem Cell Factor Improve Endogenous Repair After Myocardial Infarction." Cardiovascular Research, vol. 70, no. 1, 2006, pp. 117-25.
Kanellakis P, Slater NJ, Du XJ, et al. Granulocyte colony-stimulating factor and stem cell factor improve endogenous repair after myocardial infarction. Cardiovasc Res. 2006;70(1):117-25.
Kanellakis, P., Slater, N. J., Du, X. J., Bobik, A., & Curtis, D. J. (2006). Granulocyte colony-stimulating factor and stem cell factor improve endogenous repair after myocardial infarction. Cardiovascular Research, 70(1), 117-25.
Kanellakis P, et al. Granulocyte Colony-stimulating Factor and Stem Cell Factor Improve Endogenous Repair After Myocardial Infarction. Cardiovasc Res. 2006 Apr 1;70(1):117-25. PubMed PMID: 16497284.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Granulocyte colony-stimulating factor and stem cell factor improve endogenous repair after myocardial infarction. AU - Kanellakis,Peter, AU - Slater,Nicholas J, AU - Du,Xiao-Jun, AU - Bobik,Alex, AU - Curtis,David J, Y1 - 2006/02/23/ PY - 2005/09/09/received PY - 2006/01/05/revised PY - 2006/01/06/accepted PY - 2006/2/25/pubmed PY - 2006/8/23/medline PY - 2006/2/25/entrez SP - 117 EP - 25 JF - Cardiovascular research JO - Cardiovasc Res VL - 70 IS - 1 N2 - OBJECTIVE: The aims of this study were, first, to determine if granulocyte colony-stimulating factor (G-CSF) and stem cell factor (SCF) improved left ventricular function in the setting of a reperfusion model of myocardial infarction (MI) and, second, to evaluate the effects of G-CSF/SCF on cellular repair and, in particular, the fate of bone marrow cells homing to the site of tissue injury. METHODS: MI was induced in mice by transient ligation of the left descending coronary artery. G-CSF/SCF were administered for 5 days after MI. Cardiac function was assessed 28 days after MI. The effect of G-CSF/SCF on the cellular composition of the infarct region was assessed by immunohistochemistry. MI was performed in mice reconstituted with bone marrow cells expressing DsRed to track the fate of bone marrow-derived cells within the infarct region. RESULTS: G-CSF/SCF-treated mice had significantly improved left ventricular (LV) function as determined by LV developed pressure, LV+/-dp/dt(max/min), and LV end-diastolic pressure. G-CSF alone produced similar improvements in cardiac function. These improvements in LV function were associated with 70% more blood vessels and a doubling of cells expressing cardiomyocyte-specific transcription factors GATA-4, Nkx2.5 and alpha-actinin cells within the infarct zone. Cells within the infarct expressing stromal-derived factor also increased by 200%. To elucidate the origin of these cells, bone marrow chimeras, where hematopoietic cells expressed the fluorescent marker DsRed, were treated with G-CSF/SCF after MI. Bone marrow-derived, DsRed-expressing cells in the infarct region of G-CSF/SCF-treated chimeras increased by an average of 12-fold; however, the vast majority of DsRed cells expressed the hematopoietic-specific marker CD45 but not blood vessel or cardiomyocyte markers. CONCLUSIONS: G-CSF/SCF therapy improved cardiac function when delivered after MI, increasing the number of blood vessels and cells of cardiomyogenic lineage. However, these cells were of myocardial rather than bone marrow origin. SN - 0008-6363 UR - https://www.unboundmedicine.com/medline/citation/16497284/Granulocyte_colony_stimulating_factor_and_stem_cell_factor_improve_endogenous_repair_after_myocardial_infarction_ L2 - https://academic.oup.com/cardiovascres/article-lookup/doi/10.1016/j.cardiores.2006.01.005 DB - PRIME DP - Unbound Medicine ER -