2026-04-29T04:09:33Zhttps://repisalud.isciii.es/rest/oai/requestoai:repisalud.isciii.es:20.500.12105/52082024-09-27T09:20:19Zcom_20.500.12105_19604com_20.500.12105_2051col_20.500.12105_19605
Repisalud
author
Valiente-Alandi, I
author
Albo-Castellanos, Carmen
author
Herrero, Diego
author
Sanchez, Iria
author
Bernad, Antonio
funder
Ministerio de Ciencia e Innovación (España)
funder
Comunidad de Madrid (España)
funder
Instituto de Salud Carlos III
funder
Unión Europea. Comisión Europea
2017-10-30T13:15:41Z
2017-10-30T13:15:41Z
2016
1757-6512
http://hdl.handle.net/20.500.12105/5208
27472922
10.1186/s13287-016-0355-7
Steem Cell Research & Therapy
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.
eng
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
Bmi1(+) cardiac progenitor cells contribute to myocardial repair following acute injury
journal article
URL
https://repisalud.isciii.es/bitstreams/71be06c5-b5c0-4abd-b786-519834fe9ba1/download
File
MD5
75182b440e9a5392c745c07ec470bbe7
2770279
application/pdf
Bmi1+CardiacProgenitorCells_2016
URL
https://repisalud.isciii.es/bitstreams/839ba48a-f9a5-4f37-aac9-d0b6501e7ec7/download
File
MD5
3f782ecaf5a58a3bf899d97fa0ec4bda
45813
text/plain
Bmi1+CardiacProgenitorCells_2016.txt