G-CSF/SCF reduces inducible arrhythmias in the infarcted heart potentially via increased connexin43 expression and arteriogenesis
Granulocyte colony-stimulating factor (G-CSF), alone or in combination with stem cell factor (SCF), can improve hemodynamic cardiac function after myocardial infarction. Apart from impairing the pump function, myocardial infarction causes an enhanced vulnerability to ventricular arrhythmias. Therefo...
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| Veröffentlicht in: | The Journal of experimental medicine 2006-01, Vol.203 (1), p.87-97 |
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| creator | Kuhlmann, Michael T Kirchhof, Paulus Klocke, Rainer Hasib, Lekbira Stypmann, Jörg Fabritz, Larissa Stelljes, Matthias Tian, Wen Zwiener, Melanie Mueller, Marcus Kienast, Joachim Breithardt, Günter Nikol, Sigrid |
| description | Granulocyte colony-stimulating factor (G-CSF), alone or in combination with stem cell factor (SCF), can improve hemodynamic cardiac function after myocardial infarction. Apart from impairing the pump function, myocardial infarction causes an enhanced vulnerability to ventricular arrhythmias. Therefore, we investigated the electrophysiological effects of G-CSF/SCF and the underlying cellular events in a murine infarction model. G-CSF/SCF improved cardiac output after myocardial infarction. Although G-CSF/SCF led to a twofold increased, potentially proarrhythmic homing of bone marrow (BM)-derived cells to the area of infarction, |
| doi_str_mv | 10.1084/jem.20051151 |
| format | Article |
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Apart from impairing the pump function, myocardial infarction causes an enhanced vulnerability to ventricular arrhythmias. Therefore, we investigated the electrophysiological effects of G-CSF/SCF and the underlying cellular events in a murine infarction model. G-CSF/SCF improved cardiac output after myocardial infarction. Although G-CSF/SCF led to a twofold increased, potentially proarrhythmic homing of bone marrow (BM)-derived cells to the area of infarction, <1% of these cells adopted a cardial phenotype. Inducibility of ventricular tachycardias during programmed stimulation was reduced 5 wk after G-CSF/SCF treatment. G-CSF/SCF increased cardiomyocyte diameter, arteriogenesis, and expression of connexin43 in the border zone of the infarction. An enhanced expression of the G-CSF receptor demonstrated in cardiomyocytes and other cell types of the infarcted myocardium indicates a sensitization of the heart to direct influences of this cytokine. In addition to paracrine effects potentially caused by the increased homing of BM-derived cells, these might contribute to the therapeutic effects of G-CSF.</description><identifier>ISSN: 0022-1007</identifier><identifier>EISSN: 1540-9538</identifier><identifier>EISSN: 1892-1007</identifier><identifier>DOI: 10.1084/jem.20051151</identifier><identifier>PMID: 16401694</identifier><language>eng</language><publisher>United States: The Rockefeller University Press</publisher><subject>Animals ; Arrhythmias, Cardiac - prevention & control ; Bone Marrow Transplantation ; Cardiac Output - drug effects ; Connexin 43 - metabolism ; Disease Models, Animal ; Female ; Granulocyte Colony-Stimulating Factor - pharmacology ; Heart - physiopathology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Myocardial Infarction - metabolism ; Myocardial Infarction - physiopathology ; Myocardium - metabolism ; Myocytes, Cardiac - drug effects ; Myocytes, Cardiac - metabolism ; Neovascularization, Physiologic - drug effects ; Receptors, Granulocyte Colony-Stimulating Factor - metabolism ; Stem Cell Factor - pharmacology ; Ventricular Dysfunction, Left - metabolism ; Ventricular Dysfunction, Left - physiopathology</subject><ispartof>The Journal of experimental medicine, 2006-01, Vol.203 (1), p.87-97</ispartof><rights>Copyright © 2006, The Rockefeller University Press</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c479t-3e5458c0c5a757f7f71dc1a8e469a46e3393adae43c445bc2c3a9f3cbac536f13</citedby><cites>FETCH-LOGICAL-c479t-3e5458c0c5a757f7f71dc1a8e469a46e3393adae43c445bc2c3a9f3cbac536f13</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,776,780,881,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16401694$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kuhlmann, Michael T</creatorcontrib><creatorcontrib>Kirchhof, Paulus</creatorcontrib><creatorcontrib>Klocke, Rainer</creatorcontrib><creatorcontrib>Hasib, Lekbira</creatorcontrib><creatorcontrib>Stypmann, Jörg</creatorcontrib><creatorcontrib>Fabritz, Larissa</creatorcontrib><creatorcontrib>Stelljes, Matthias</creatorcontrib><creatorcontrib>Tian, Wen</creatorcontrib><creatorcontrib>Zwiener, Melanie</creatorcontrib><creatorcontrib>Mueller, Marcus</creatorcontrib><creatorcontrib>Kienast, Joachim</creatorcontrib><creatorcontrib>Breithardt, Günter</creatorcontrib><creatorcontrib>Nikol, Sigrid</creatorcontrib><title>G-CSF/SCF reduces inducible arrhythmias in the infarcted heart potentially via increased connexin43 expression and arteriogenesis</title><title>The Journal of experimental medicine</title><addtitle>J Exp Med</addtitle><description>Granulocyte colony-stimulating factor (G-CSF), alone or in combination with stem cell factor (SCF), can improve hemodynamic cardiac function after myocardial infarction. Apart from impairing the pump function, myocardial infarction causes an enhanced vulnerability to ventricular arrhythmias. Therefore, we investigated the electrophysiological effects of G-CSF/SCF and the underlying cellular events in a murine infarction model. G-CSF/SCF improved cardiac output after myocardial infarction. Although G-CSF/SCF led to a twofold increased, potentially proarrhythmic homing of bone marrow (BM)-derived cells to the area of infarction, <1% of these cells adopted a cardial phenotype. Inducibility of ventricular tachycardias during programmed stimulation was reduced 5 wk after G-CSF/SCF treatment. G-CSF/SCF increased cardiomyocyte diameter, arteriogenesis, and expression of connexin43 in the border zone of the infarction. An enhanced expression of the G-CSF receptor demonstrated in cardiomyocytes and other cell types of the infarcted myocardium indicates a sensitization of the heart to direct influences of this cytokine. In addition to paracrine effects potentially caused by the increased homing of BM-derived cells, these might contribute to the therapeutic effects of G-CSF.</description><subject>Animals</subject><subject>Arrhythmias, Cardiac - prevention & control</subject><subject>Bone Marrow Transplantation</subject><subject>Cardiac Output - drug effects</subject><subject>Connexin 43 - metabolism</subject><subject>Disease Models, Animal</subject><subject>Female</subject><subject>Granulocyte Colony-Stimulating Factor - pharmacology</subject><subject>Heart - physiopathology</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Transgenic</subject><subject>Myocardial Infarction - metabolism</subject><subject>Myocardial Infarction - physiopathology</subject><subject>Myocardium - metabolism</subject><subject>Myocytes, Cardiac - drug effects</subject><subject>Myocytes, Cardiac - metabolism</subject><subject>Neovascularization, Physiologic - drug effects</subject><subject>Receptors, Granulocyte Colony-Stimulating Factor - metabolism</subject><subject>Stem Cell Factor - pharmacology</subject><subject>Ventricular Dysfunction, Left - metabolism</subject><subject>Ventricular Dysfunction, Left - physiopathology</subject><issn>0022-1007</issn><issn>1540-9538</issn><issn>1892-1007</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkc1v1DAQxS0EokvhxhnlxIm0ntiOkwsSWrEFqRKHwtmadSaNq8RebG_VPfKf41WXrxOaw5PmPf00o8fYa-AXwDt5eUfLRcO5AlDwhK1ASV73SnRP2YrzpqmBc33GXqR0xzlIqdrn7AxayaHt5Yr9uKrXN5vLm_WmijTsLaXK-aJuO1OFMU6HPC0Oj9sqT1RkxGgzDdVEGHO1C5l8djjPh-reYfFtJEzFt8F7enBeiooedpFScsFX6IeCzRRduCVPyaWX7NmIc6JXJz1n3zYfv64_1ddfrj6vP1zXVuo-14KUVJ3lVqFWeiwDgwXsSLY9ypaE6AUOSFLY8uTWNlZgPwq7RatEO4I4Z-8fubv9dqHBlrMjzmYX3YLxYAI686_j3WRuw71pADreNgXw9gSI4fueUjaLS5bmGT2FfTKaa2g7rv8bBC01b_SR-O4xaGNIKdL4-xrg5liuKeWaX-WW-Ju_P_gTPrUpfgKZNaOG</recordid><startdate>20060123</startdate><enddate>20060123</enddate><creator>Kuhlmann, Michael T</creator><creator>Kirchhof, Paulus</creator><creator>Klocke, Rainer</creator><creator>Hasib, Lekbira</creator><creator>Stypmann, Jörg</creator><creator>Fabritz, Larissa</creator><creator>Stelljes, Matthias</creator><creator>Tian, Wen</creator><creator>Zwiener, Melanie</creator><creator>Mueller, Marcus</creator><creator>Kienast, Joachim</creator><creator>Breithardt, Günter</creator><creator>Nikol, Sigrid</creator><general>The Rockefeller University Press</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7T5</scope><scope>H94</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20060123</creationdate><title>G-CSF/SCF reduces inducible arrhythmias in the infarcted heart potentially via increased connexin43 expression and arteriogenesis</title><author>Kuhlmann, Michael T ; Kirchhof, Paulus ; Klocke, Rainer ; Hasib, Lekbira ; Stypmann, Jörg ; Fabritz, Larissa ; Stelljes, Matthias ; Tian, Wen ; Zwiener, Melanie ; Mueller, Marcus ; Kienast, Joachim ; Breithardt, Günter ; Nikol, Sigrid</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c479t-3e5458c0c5a757f7f71dc1a8e469a46e3393adae43c445bc2c3a9f3cbac536f13</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Animals</topic><topic>Arrhythmias, Cardiac - prevention & control</topic><topic>Bone Marrow Transplantation</topic><topic>Cardiac Output - drug effects</topic><topic>Connexin 43 - metabolism</topic><topic>Disease Models, Animal</topic><topic>Female</topic><topic>Granulocyte Colony-Stimulating Factor - pharmacology</topic><topic>Heart - physiopathology</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Transgenic</topic><topic>Myocardial Infarction - metabolism</topic><topic>Myocardial Infarction - physiopathology</topic><topic>Myocardium - metabolism</topic><topic>Myocytes, Cardiac - drug effects</topic><topic>Myocytes, Cardiac - metabolism</topic><topic>Neovascularization, Physiologic - drug effects</topic><topic>Receptors, Granulocyte Colony-Stimulating Factor - metabolism</topic><topic>Stem Cell Factor - pharmacology</topic><topic>Ventricular Dysfunction, Left - metabolism</topic><topic>Ventricular Dysfunction, Left - physiopathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kuhlmann, Michael T</creatorcontrib><creatorcontrib>Kirchhof, Paulus</creatorcontrib><creatorcontrib>Klocke, Rainer</creatorcontrib><creatorcontrib>Hasib, Lekbira</creatorcontrib><creatorcontrib>Stypmann, Jörg</creatorcontrib><creatorcontrib>Fabritz, Larissa</creatorcontrib><creatorcontrib>Stelljes, Matthias</creatorcontrib><creatorcontrib>Tian, Wen</creatorcontrib><creatorcontrib>Zwiener, Melanie</creatorcontrib><creatorcontrib>Mueller, Marcus</creatorcontrib><creatorcontrib>Kienast, Joachim</creatorcontrib><creatorcontrib>Breithardt, Günter</creatorcontrib><creatorcontrib>Nikol, Sigrid</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>The Journal of experimental medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kuhlmann, Michael T</au><au>Kirchhof, Paulus</au><au>Klocke, Rainer</au><au>Hasib, Lekbira</au><au>Stypmann, Jörg</au><au>Fabritz, Larissa</au><au>Stelljes, Matthias</au><au>Tian, Wen</au><au>Zwiener, Melanie</au><au>Mueller, Marcus</au><au>Kienast, Joachim</au><au>Breithardt, Günter</au><au>Nikol, Sigrid</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>G-CSF/SCF reduces inducible arrhythmias in the infarcted heart potentially via increased connexin43 expression and arteriogenesis</atitle><jtitle>The Journal of experimental medicine</jtitle><addtitle>J Exp Med</addtitle><date>2006-01-23</date><risdate>2006</risdate><volume>203</volume><issue>1</issue><spage>87</spage><epage>97</epage><pages>87-97</pages><issn>0022-1007</issn><eissn>1540-9538</eissn><eissn>1892-1007</eissn><abstract>Granulocyte colony-stimulating factor (G-CSF), alone or in combination with stem cell factor (SCF), can improve hemodynamic cardiac function after myocardial infarction. Apart from impairing the pump function, myocardial infarction causes an enhanced vulnerability to ventricular arrhythmias. Therefore, we investigated the electrophysiological effects of G-CSF/SCF and the underlying cellular events in a murine infarction model. G-CSF/SCF improved cardiac output after myocardial infarction. Although G-CSF/SCF led to a twofold increased, potentially proarrhythmic homing of bone marrow (BM)-derived cells to the area of infarction, <1% of these cells adopted a cardial phenotype. Inducibility of ventricular tachycardias during programmed stimulation was reduced 5 wk after G-CSF/SCF treatment. G-CSF/SCF increased cardiomyocyte diameter, arteriogenesis, and expression of connexin43 in the border zone of the infarction. An enhanced expression of the G-CSF receptor demonstrated in cardiomyocytes and other cell types of the infarcted myocardium indicates a sensitization of the heart to direct influences of this cytokine. In addition to paracrine effects potentially caused by the increased homing of BM-derived cells, these might contribute to the therapeutic effects of G-CSF.</abstract><cop>United States</cop><pub>The Rockefeller University Press</pub><pmid>16401694</pmid><doi>10.1084/jem.20051151</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | The Journal of experimental medicine, 2006-01, Vol.203 (1), p.87-97 |
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| subjects | Animals Arrhythmias, Cardiac - prevention & control Bone Marrow Transplantation Cardiac Output - drug effects Connexin 43 - metabolism Disease Models, Animal Female Granulocyte Colony-Stimulating Factor - pharmacology Heart - physiopathology Male Mice Mice, Inbred C57BL Mice, Transgenic Myocardial Infarction - metabolism Myocardial Infarction - physiopathology Myocardium - metabolism Myocytes, Cardiac - drug effects Myocytes, Cardiac - metabolism Neovascularization, Physiologic - drug effects Receptors, Granulocyte Colony-Stimulating Factor - metabolism Stem Cell Factor - pharmacology Ventricular Dysfunction, Left - metabolism Ventricular Dysfunction, Left - physiopathology |
| title | G-CSF/SCF reduces inducible arrhythmias in the infarcted heart potentially via increased connexin43 expression and arteriogenesis |
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