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Although the heart is one of the least regenerative organs in the body, evidence accumulated in recent decades indicates a certain degree of renewal after injury. We have evaluated the role of cardiac <jats:italic>Bmi1<\/jats:italic><jats:sup>\n                    <jats:italic>+<\/jats:italic>\n                  <\/jats:sup> progenitor cells (<jats:italic>Bmi1<\/jats:italic>-CPC) following acute myocardial infarction (AMI).<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Methods<\/jats:title>\n                <jats:p><jats:italic>Bmi1<\/jats:italic><jats:sup>Cre\/+<\/jats:sup>;<jats:italic>Rosa26<\/jats:italic><jats:sup>YFP\/+<\/jats:sup> (<jats:italic>Bmi1<\/jats:italic>-YFP) mice were used for lineage tracing strategy. After tamoxifen (TM) induction, yellow fluorescent protein (YFP) is expressed under the control of <jats:italic>Rosa26<\/jats:italic> regulatory sequences in <jats:italic>Bmi1<\/jats:italic><jats:sup>\n                    <jats:italic>+<\/jats:italic>\n                  <\/jats:sup> cells. YFP<jats:sup>+<\/jats:sup> cells were tracked following myocardial infarction. Additionally, whole transcriptome analysis of isolated YFP<jats:sup>+<\/jats:sup> cells was performed in unchallenged hearts and after myocardial infarction.<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Results<\/jats:title>\n                <jats:p>Deep-sequencing analysis of <jats:italic>Bmi1<\/jats:italic>-CPC from unchallenged hearts suggests that this population expresses high levels of pluripotency markers. Conversely, transcriptome evaluation of <jats:italic>Bmi1<\/jats:italic>-CPC following AMI shows a rich representation of genes related to cell proliferation, movement, and cell cycle. Lineage-tracing studies after cardiac infarction show that the progeny of <jats:italic>Bmi1<\/jats:italic>-expressing cells contribute to de novo cardiomyocytes (CM) (13.8\u2009\u00b1\u20095 % new YFP<jats:sup>+<\/jats:sup> CM compared to 4.7\u2009\u00b1\u20090.9 % in age-paired non-infarcted hearts). However, apical resection of TM-induced day 1 <jats:italic>Bmi1<\/jats:italic>-YFP pups indicated a very minor contribution of <jats:italic>Bmi1<\/jats:italic>-derived cells to de novo CM.<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Conclusions<\/jats:title>\n                <jats:p>Cardiac <jats:italic>Bmi1<\/jats:italic> progenitor cells respond to cardiac injury, contributing to the generation of de novo CM in the adult mouse heart.<\/jats:p>\n              <\/jats:sec>","DOI":"10.1186\/s13287-016-0355-7","type":"journal-article","created":{"date-parts":[[2016,7,30]],"date-time":"2016-07-30T00:50:22Z","timestamp":1469839822000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":41,"title":["Bmi1\n                     + cardiac progenitor cells contribute to myocardial repair following acute injury"],"prefix":"10.1186","volume":"7","author":[{"given":"I\u00f1igo","family":"Valiente-Alandi","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Carmen","family":"Albo-Castellanos","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Diego","family":"Herrero","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Iria","family":"Sanchez","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Antonio","family":"Bernad","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"297","published-online":{"date-parts":[[2016,7,30]]},"reference":[{"key":"355_CR1","doi-asserted-by":"publisher","first-page":"326","DOI":"10.1038\/nature10147","volume":"473","author":"MA Laflamme","year":"2011","unstructured":"Laflamme MA, Murry CE. 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