{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,4]],"date-time":"2026-10-04T18:16:43Z","timestamp":1791137803254,"version":"4.1.0"},"reference-count":45,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2008,9,30]],"date-time":"2008-09-30T00:00:00Z","timestamp":1222732800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["faseb.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["The FASEB Journal"],"published-print":{"date-parts":[[2009,2]]},"abstract":"<jats:p>\n                    Mobilization of bone marrow\u2010derived stem cells (BMCs) was shown to have protective effects after myocardial infarction (MI). However, the classical mobilizing agent, granulocyte\u2010colony stimulating factor (G\u2010CSF) relapsed after revealing an impaired homing capacity. In the search for superior cytokines, erythropoietin (EPO) appears to be a promising agent. Therefore, we analyzed in a murine model of surgically induced MI the influence of EPO treatment on survival and functional parameters as well as BMC mobilization, homing, and effect on resident cardiac stem cells (CSCs). Human EPO was injected intraperitoneally after ligation of the left anterior descendens (LAD) for 3 days with a total dose of 5000 IU\/kg 6 and 30 days after MI, and pressure volume relationships were investigated\n                    <jats:italic>in vivo<\/jats:italic>\n                    . Cardiac tissues were analyzed by histology. To show the effect on BMCs and CSCs, FACS analyses were performed. Homing factors were analyzed by quantitative reverse transcription\u2010polymerase chain reaction (qRT\u2010PCR) and ELISA. EPO\u2010treated animals showed a significant improvement of survival post\u2010MI (62\n                    <jats:italic>vs<\/jats:italic>\n                    . 36%). At days 6 and 30, all hemodynamic parameters associated with attenuated remodeling, enhanced neovascularization, and diminished apoptotic cells in the peri\u2010infarct area were improved. BMC subpopulations (CD31\n                    <jats:sup>+<\/jats:sup>\n                    , c\u2010kit\n                    <jats:sup>+<\/jats:sup>\n                    , and Sca\u20101\n                    <jats:sup>+<\/jats:sup>\n                    cells) were mobilized, and homing of Sca\u20101\n                    <jats:sup>+<\/jats:sup>\n                    and CXCR4\n                    <jats:sup>+<\/jats:sup>\n                    BMCs toward an SDF\u20101 gradient into the ischemic myocardium was enhanced. However, there was no beneficial effect on CSCs. We have shown that EPO application after MI shows cardioprotective effects. This may be explained by mobilization of BMCs, which are homing\n                    <jats:italic>via<\/jats:italic>\n                    the CXCR\u20104\/SDF\u20101 axis. However, EPO has no beneficial effects on resident CSCs. Therefore, new treatment regimes using EPO together with other agents may combine complementary beneficial effects preventing ischemic cardiomyopathy.\u2014Brunner, S., Winogradow, J., Huber, B. C, Zaruba, M.\u2010M., Fischer, R, David, R, Assmann, G., Herbach, N., Wanke, R, Mueller\u2010Hoecker, J., Franz, W.\u2010M. Erythropoietin administration after myocardial infarction in mice attenuates ischemic cardiomyopathy associated with enhanced homing of bone marrow\u2010derived progenitor cells\n                    <jats:italic>via<\/jats:italic>\n                    the CXCR\u20104\/SDF\u20101 axis.\n                    <jats:italic>FASEB J<\/jats:italic>\n                    . 23, 351\u2013361 (2009)\n                  <\/jats:p>","DOI":"10.1096\/fj.08-109462","type":"journal-article","created":{"date-parts":[[2008,9,30]],"date-time":"2008-09-30T22:53:55Z","timestamp":1222815235000},"page":"351-361","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":79,"title":["Erythropoietin administration after myocardial infarction in mice attenuates ischemic cardiomyopathy associated with enhanced homing of bone marrow\u2010derived progenitor cells\n                    <i>via<\/i>\n                    the CXCR\u20104\/SDF\u20101 axis"],"prefix":"10.1096","volume":"23","author":[{"given":"Stefan","family":"Brunner","sequence":"first","affiliation":[{"name":"Klinikum Grosshadern, Medical Department I Ludwig\u2010Maximilians\u2010University Munich Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Janina","family":"Winogradow","sequence":"additional","affiliation":[{"name":"Klinikum Grosshadern, Medical Department I Ludwig\u2010Maximilians\u2010University Munich Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bruno C.","family":"Huber","sequence":"additional","affiliation":[{"name":"Klinikum Grosshadern, Medical Department I Ludwig\u2010Maximilians\u2010University Munich Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marc\u2010Michael","family":"Zaruba","sequence":"additional","affiliation":[{"name":"Klinikum Grosshadern, Medical Department I Ludwig\u2010Maximilians\u2010University Munich Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rebekka","family":"Fischer","sequence":"additional","affiliation":[{"name":"Klinikum Grosshadern, Medical Department I Ludwig\u2010Maximilians\u2010University Munich Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Robert","family":"David","sequence":"additional","affiliation":[{"name":"Klinikum Grosshadern, Medical Department I Ludwig\u2010Maximilians\u2010University Munich Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gerald","family":"Assmann","sequence":"additional","affiliation":[{"name":"Institute of Pathology Ludwig\u2010Maximilians\u2010University Munich Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nadja","family":"Herbach","sequence":"additional","affiliation":[{"name":"Institute of Veterinary Pathology Ludwig\u2010Maximilians\u2010University Munich Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ruediger","family":"Wanke","sequence":"additional","affiliation":[{"name":"Institute of Veterinary Pathology Ludwig\u2010Maximilians\u2010University Munich Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Josef","family":"Mueller\u2010Hoecker","sequence":"additional","affiliation":[{"name":"Institute of Pathology Ludwig\u2010Maximilians\u2010University Munich Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wolfgang\u2010Michael","family":"Franz","sequence":"additional","affiliation":[{"name":"Klinikum Grosshadern, Medical Department I Ludwig\u2010Maximilians\u2010University Munich Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2008,9,30]]},"reference":[{"key":"e_1_2_6_2_1","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.0000134791.68010.FA"},{"key":"e_1_2_6_3_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.jacc.2004.08.014"},{"key":"e_1_2_6_4_1","first-page":"396","article-title":"Stem cell therapy after myocardial infarction: ready for clinical application?","volume":"8","author":"Engelmann M. 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