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G-CSF treatment after myocardial infarction: impact on bone marrow-derived vs cardiac progenitor cells.
Exp Hematol. 2008 Jun; 36(6):695-702.EH

Abstract

OBJECTIVE

Besides its classical function in the field of autologous and allogenic stem cell transplantation, granulocyte colony-stimulating factor (G-CSF) was shown to have protective effects after myocardial infarction (MI) by mobilization of bone marrow-derived progenitor cells (BMCs) and in addition by activation of multiple signaling pathways. In the present study, we focused on the impact of G-CSF on migration of BMCs and the impact on resident cardiac cells after MI.

MATERIALS AND METHODS

Mice (C57BL/6J) were sublethally irradiated, and BM from green fluorescent protein (GFP)-transgenic mice was transplanted. Coronary artery ligation was performed 10 weeks later. G-CSF (100 microg/kg) was daily injected for 6 days. Subpopulations of enhanced GFP(+) cells in peripheral blood, bone marrow, and heart were characterized by flow cytometry. Growth factor expression in the heart was analyzed by quantitative real-time polymerase chain reaction. Perfusion was investigated in vivo by gated single photon emission computed tomography (SPECT).

RESULTS

G-CSF-treated animals revealed a reduced migration of c-kit(+) and CXCR-4(+) BMCs associated with decreased expression levels of the corresponding growth factors, namely stem cell factor and stromal-derived factor-1 alpha in ischemic myocardium. In contrast, the number of resident cardiac Sca-1(+) cells was significantly increased. However, SPECT-perfusion showed no differences in infarct size between G-CSF-treated and control animals 6 days after MI.

CONCLUSION

Our study shows that G-CSF treatment after MI reduces migration capacity of BMCs into ischemic tissue, but increases the number of resident cardiac cells. To optimize homing capacity a combination of G-CSF with other agents may optimize cytokine therapy after MI.

Authors+Show Affiliations

Ludwig-Maximilians-University, Klinikum Grosshadern, Medical Department I, Munich, Germany.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo 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

18346841

Citation

Brunner, Stefan, et al. "G-CSF Treatment After Myocardial Infarction: Impact On Bone Marrow-derived Vs Cardiac Progenitor Cells." Experimental Hematology, vol. 36, no. 6, 2008, pp. 695-702.
Brunner S, Huber BC, Fischer R, et al. G-CSF treatment after myocardial infarction: impact on bone marrow-derived vs cardiac progenitor cells. Exp Hematol. 2008;36(6):695-702.
Brunner, S., Huber, B. C., Fischer, R., Groebner, M., Hacker, M., David, R., Zaruba, M. M., Vallaster, M., Rischpler, C., Wilke, A., Gerbitz, A., & Franz, W. M. (2008). G-CSF treatment after myocardial infarction: impact on bone marrow-derived vs cardiac progenitor cells. Experimental Hematology, 36(6), 695-702. https://doi.org/10.1016/j.exphem.2008.01.011
Brunner S, et al. G-CSF Treatment After Myocardial Infarction: Impact On Bone Marrow-derived Vs Cardiac Progenitor Cells. Exp Hematol. 2008;36(6):695-702. PubMed PMID: 18346841.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - G-CSF treatment after myocardial infarction: impact on bone marrow-derived vs cardiac progenitor cells. AU - Brunner,Stefan, AU - Huber,Bruno C, AU - Fischer,Rebekka, AU - Groebner,Michael, AU - Hacker,Marcus, AU - David,Robert, AU - Zaruba,Marc-Michael, AU - Vallaster,Marcus, AU - Rischpler,Christoph, AU - Wilke,Andrea, AU - Gerbitz,Armin, AU - Franz,Wolfgang-Michael, Y1 - 2008/03/17/ PY - 2007/10/31/received PY - 2007/10/31/revised PY - 2008/01/23/accepted PY - 2008/3/19/pubmed PY - 2008/8/6/medline PY - 2008/3/19/entrez SP - 695 EP - 702 JF - Experimental hematology JO - Exp Hematol VL - 36 IS - 6 N2 - OBJECTIVE: Besides its classical function in the field of autologous and allogenic stem cell transplantation, granulocyte colony-stimulating factor (G-CSF) was shown to have protective effects after myocardial infarction (MI) by mobilization of bone marrow-derived progenitor cells (BMCs) and in addition by activation of multiple signaling pathways. In the present study, we focused on the impact of G-CSF on migration of BMCs and the impact on resident cardiac cells after MI. MATERIALS AND METHODS: Mice (C57BL/6J) were sublethally irradiated, and BM from green fluorescent protein (GFP)-transgenic mice was transplanted. Coronary artery ligation was performed 10 weeks later. G-CSF (100 microg/kg) was daily injected for 6 days. Subpopulations of enhanced GFP(+) cells in peripheral blood, bone marrow, and heart were characterized by flow cytometry. Growth factor expression in the heart was analyzed by quantitative real-time polymerase chain reaction. Perfusion was investigated in vivo by gated single photon emission computed tomography (SPECT). RESULTS: G-CSF-treated animals revealed a reduced migration of c-kit(+) and CXCR-4(+) BMCs associated with decreased expression levels of the corresponding growth factors, namely stem cell factor and stromal-derived factor-1 alpha in ischemic myocardium. In contrast, the number of resident cardiac Sca-1(+) cells was significantly increased. However, SPECT-perfusion showed no differences in infarct size between G-CSF-treated and control animals 6 days after MI. CONCLUSION: Our study shows that G-CSF treatment after MI reduces migration capacity of BMCs into ischemic tissue, but increases the number of resident cardiac cells. To optimize homing capacity a combination of G-CSF with other agents may optimize cytokine therapy after MI. SN - 0301-472X UR - https://www.unboundmedicine.com/medline/citation/18346841/G_CSF_treatment_after_myocardial_infarction:_impact_on_bone_marrow_derived_vs_cardiac_progenitor_cells_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0301-472X(08)00047-7 DB - PRIME DP - Unbound Medicine ER -