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...

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Detalles Bibliográficos
Autores: Valiente-Alandi, I, Albo-Castellanos, Carmen, Herrero, Diego, Sanchez, Iria, Bernad, Antonio
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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oai_identifier_str oai:repisalud.isciii.es:20.500.12105/5208
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repository_id_str
spelling 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
repository.name.fl_str_mv
repository.mail.fl_str_mv
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