Bmi1(+) cardiac progenitor cells contribute to myocardial repair following acute injury
Background: The inability of the adult mammalian heart to replace cells lost after severe cardiac injury compromises organ function. 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 h...
| Autores: | , , , , |
|---|---|
| Tipo de recurso: | artículo |
| Fecha de publicación: | 2016 |
| País: | España |
| Institución: | Instituto de Salud Carlos III (ISCIII) |
| Repositorio: | Repisalud |
| Idioma: | inglés |
| OAI Identifier: | oai:repisalud.isciii.es:20.500.12105/5208 |
| Acceso en línea: | http://hdl.handle.net/20.500.12105/5208 |
| Access Level: | acceso abierto |
| Palabra clave: | Myocardial infarction Stem cells Bmi1 Cardiac progenitor cells ZEBRAFISH HEART REGENERATION MURINE ADULT HEART STEM-CELLS NEONATAL HEART C-KIT(+) CELLS MOUSE HEART IN-VIVO CARDIOMYOCYTES RENEWAL PROLIFERATION |
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Bmi1(+) cardiac progenitor cells contribute to myocardial repair following acute injuryValiente-Alandi, IAlbo-Castellanos, CarmenHerrero, DiegoSanchez, IriaBernad, AntonioMyocardial infarctionStem cellsBmi1Cardiac progenitor cellsZEBRAFISH HEART REGENERATIONMURINE ADULT HEARTSTEM-CELLSNEONATAL HEARTC-KIT(+) CELLSMOUSE HEARTIN-VIVOCARDIOMYOCYTESRENEWALPROLIFERATIONBackground: The inability of the adult mammalian heart to replace cells lost after severe cardiac injury compromises organ function. 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 Bmi1(+) progenitor cells (Bmi1-CPC) following acute myocardial infarction (AMI). Methods: Bmi1(Cre/+); Rosa26(YFP/+) (Bmi1-YFP) mice were used for lineage tracing strategy. After tamoxifen (TM) induction, yellow fluorescent protein (YFP) is expressed under the control of Rosa26 regulatory sequences in Bmi1(+) cells. YFP+ cells were tracked following myocardial infarction. Additionally, whole transcriptome analysis of isolated YFP+ cells was performed in unchallenged hearts and after myocardial infarction. Results: Deep-sequencing analysis of Bmi1-CPC from unchallenged hearts suggests that this population expresses high levels of pluripotency markers. Conversely, transcriptome evaluation of Bmi1-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 Bmi1-expressing cells contribute to de novo cardiomyocytes (CM) (13.8 +/- 5 \% new YFP+ CM compared to 4.7 +/- 0.9 \% in age-paired non-infarcted hearts). However, apical resection of TM-induced day 1 Bmi1-YFP pups indicated a very minor contribution of Bmi1-derived cells to de novo CM. Conclusions: Cardiac Bmi1 progenitor cells respond to cardiac injury, contributing to the generation of de novo CM in the adult mouse heart.BioMed Central (BMC)Ministerio de Ciencia e Innovación (España)Comunidad de Madrid (España)Instituto de Salud Carlos IIIUnión Europea. Comisión Europea20172017-10-3020162016-01-0120162016-01-01journal articlehttp://purl.org/coar/resource_type/c_6501VoRhttp://purl.org/coar/version/c_970fb48d4fbd8a85info:eu-repo/semantics/articleapplication/pdfhttp://hdl.handle.net/20.500.12105/5208reponame:Repisaludinstname:Instituto de Salud Carlos III (ISCIII)Inglésengopen accesshttp://purl.org/coar/access_right/c_abf2Atribución 4.0 Internacionalhttp://creativecommons.org/licenses/by/4.0/info:eu-repo/semantics/openAccessoai:repisalud.isciii.es:20.500.12105/52082026-06-12T12:43:37Z |
| dc.title.none.fl_str_mv |
Bmi1(+) cardiac progenitor cells contribute to myocardial repair following acute injury |
| title |
Bmi1(+) cardiac progenitor cells contribute to myocardial repair following acute injury |
| spellingShingle |
Bmi1(+) cardiac progenitor cells contribute to myocardial repair following acute injury Valiente-Alandi, I Myocardial infarction Stem cells Bmi1 Cardiac progenitor cells ZEBRAFISH HEART REGENERATION MURINE ADULT HEART STEM-CELLS NEONATAL HEART C-KIT(+) CELLS MOUSE HEART IN-VIVO CARDIOMYOCYTES RENEWAL PROLIFERATION |
| title_short |
Bmi1(+) cardiac progenitor cells contribute to myocardial repair following acute injury |
| title_full |
Bmi1(+) cardiac progenitor cells contribute to myocardial repair following acute injury |
| title_fullStr |
Bmi1(+) cardiac progenitor cells contribute to myocardial repair following acute injury |
| title_full_unstemmed |
Bmi1(+) cardiac progenitor cells contribute to myocardial repair following acute injury |
| title_sort |
Bmi1(+) cardiac progenitor cells contribute to myocardial repair following acute injury |
| dc.creator.none.fl_str_mv |
Valiente-Alandi, I Albo-Castellanos, Carmen Herrero, Diego Sanchez, Iria Bernad, Antonio |
| author |
Valiente-Alandi, I |
| author_facet |
Valiente-Alandi, I Albo-Castellanos, Carmen Herrero, Diego Sanchez, Iria Bernad, Antonio |
| author_role |
author |
| author2 |
Albo-Castellanos, Carmen Herrero, Diego Sanchez, Iria Bernad, Antonio |
| author2_role |
author author author author |
| dc.contributor.none.fl_str_mv |
Ministerio de Ciencia e Innovación (España) Comunidad de Madrid (España) Instituto de Salud Carlos III Unión Europea. Comisión Europea |
| dc.subject.none.fl_str_mv |
Myocardial infarction Stem cells Bmi1 Cardiac progenitor cells ZEBRAFISH HEART REGENERATION MURINE ADULT HEART STEM-CELLS NEONATAL HEART C-KIT(+) CELLS MOUSE HEART IN-VIVO CARDIOMYOCYTES RENEWAL PROLIFERATION |
| topic |
Myocardial infarction Stem cells Bmi1 Cardiac progenitor cells ZEBRAFISH HEART REGENERATION MURINE ADULT HEART STEM-CELLS NEONATAL HEART C-KIT(+) CELLS MOUSE HEART IN-VIVO CARDIOMYOCYTES RENEWAL PROLIFERATION |
| description |
Background: The inability of the adult mammalian heart to replace cells lost after severe cardiac injury compromises organ function. 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 Bmi1(+) progenitor cells (Bmi1-CPC) following acute myocardial infarction (AMI). Methods: Bmi1(Cre/+); Rosa26(YFP/+) (Bmi1-YFP) mice were used for lineage tracing strategy. After tamoxifen (TM) induction, yellow fluorescent protein (YFP) is expressed under the control of Rosa26 regulatory sequences in Bmi1(+) cells. YFP+ cells were tracked following myocardial infarction. Additionally, whole transcriptome analysis of isolated YFP+ cells was performed in unchallenged hearts and after myocardial infarction. Results: Deep-sequencing analysis of Bmi1-CPC from unchallenged hearts suggests that this population expresses high levels of pluripotency markers. Conversely, transcriptome evaluation of Bmi1-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 Bmi1-expressing cells contribute to de novo cardiomyocytes (CM) (13.8 +/- 5 \% new YFP+ CM compared to 4.7 +/- 0.9 \% in age-paired non-infarcted hearts). However, apical resection of TM-induced day 1 Bmi1-YFP pups indicated a very minor contribution of Bmi1-derived cells to de novo CM. Conclusions: Cardiac Bmi1 progenitor cells respond to cardiac injury, contributing to the generation of de novo CM in the adult mouse heart. |
| publishDate |
2016 |
| dc.date.none.fl_str_mv |
2016 2016-01-01 2016 2016-01-01 2017 2017-10-30 |
| dc.type.none.fl_str_mv |
journal article http://purl.org/coar/resource_type/c_6501 VoR http://purl.org/coar/version/c_970fb48d4fbd8a85 |
| dc.type.openaire.fl_str_mv |
info:eu-repo/semantics/article |
| format |
article |
| dc.identifier.none.fl_str_mv |
http://hdl.handle.net/20.500.12105/5208 |
| url |
http://hdl.handle.net/20.500.12105/5208 |
| dc.language.none.fl_str_mv |
Inglés eng |
| language_invalid_str_mv |
Inglés |
| language |
eng |
| dc.rights.none.fl_str_mv |
open access http://purl.org/coar/access_right/c_abf2 Atribución 4.0 Internacional http://creativecommons.org/licenses/by/4.0/ |
| dc.rights.openaire.fl_str_mv |
info:eu-repo/semantics/openAccess |
| rights_invalid_str_mv |
open access http://purl.org/coar/access_right/c_abf2 Atribución 4.0 Internacional http://creativecommons.org/licenses/by/4.0/ |
| eu_rights_str_mv |
openAccess |
| dc.format.none.fl_str_mv |
application/pdf |
| dc.publisher.none.fl_str_mv |
BioMed Central (BMC) |
| publisher.none.fl_str_mv |
BioMed Central (BMC) |
| dc.source.none.fl_str_mv |
reponame:Repisalud instname:Instituto de Salud Carlos III (ISCIII) |
| instname_str |
Instituto de Salud Carlos III (ISCIII) |
| reponame_str |
Repisalud |
| collection |
Repisalud |
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|
| repository.mail.fl_str_mv |
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1869422083523477504 |
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15,812429 |