PMID- 25199831
OWN - NLM
STAT- MEDLINE
DCOM- 20150603
LR  - 20170926
IS  - 2211-1247 (Electronic)
VI  - 8
IP  - 6
DP  - 2014 Sep 25
TI  - Cell competition promotes phenotypically silent cardiomyocyte replacement in the 
      mammalian heart.
PG  - 1741-1751
LID - S2211-1247(14)00668-8 [pii]
LID - 10.1016/j.celrep.2014.08.005 [doi]
AB  - Heterogeneous anabolic capacity in cell populations can trigger a phenomenon 
      known as cell competition, through which less active cells are eliminated. Cell 
      competition has been induced experimentally in stem/precursor cell populations in 
      insects and mammals and takes place endogenously in early mouse embryonic cells. 
      Here, we show that cell competition can be efficiently induced in mouse 
      cardiomyocytes by mosaic overexpression of Myc during both gestation and adult 
      life. The expansion of the Myc-overexpressing cardiomyocyte population is driven 
      by the elimination of wild-type cardiomyocytes. Importantly, this cardiomyocyte 
      replacement is phenotypically silent and does not affect heart anatomy or 
      function. These results show that the capacity for cell competition in mammals is 
      not restricted to stem cell populations and suggest that stimulated cell 
      competition has potential as a cardiomyocyte-replacement strategy.
CI  - Copyright (c) 2014 The Authors. Published by Elsevier Inc. All rights reserved.
FAU - Villa Del Campo, Cristina
AU  - Villa Del Campo C
AD  - Departamento de Desarrollo y Reparacion Cardiovascular, Centro Nacional de 
      Investigaciones Cardiovasculares (CNIC), c/ Melchor Fernandez Almagro, 3, E-28029 
      Madrid, Spain.
FAU - Claveria, Cristina
AU  - Claveria C
AD  - Departamento de Desarrollo y Reparacion Cardiovascular, Centro Nacional de 
      Investigaciones Cardiovasculares (CNIC), c/ Melchor Fernandez Almagro, 3, E-28029 
      Madrid, Spain.
FAU - Sierra, Rocio
AU  - Sierra R
AD  - Departamento de Desarrollo y Reparacion Cardiovascular, Centro Nacional de 
      Investigaciones Cardiovasculares (CNIC), c/ Melchor Fernandez Almagro, 3, E-28029 
      Madrid, Spain.
FAU - Torres, Miguel
AU  - Torres M
AD  - Departamento de Desarrollo y Reparacion Cardiovascular, Centro Nacional de 
      Investigaciones Cardiovasculares (CNIC), c/ Melchor Fernandez Almagro, 3, E-28029 
      Madrid, Spain. Electronic address: mtorres@cnic.es.
LA  - eng
SI  - GEO/GSE58858
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20140904
PL  - United States
TA  - Cell Rep
JT  - Cell reports
JID - 101573691
RN  - 0 (Homeobox Protein Nkx-2.5)
RN  - 0 (Homeodomain Proteins)
RN  - 0 (LIM-Homeodomain Proteins)
RN  - 0 (Nkx2-5 protein, mouse)
RN  - 0 (Proto-Oncogene Proteins c-myc)
RN  - 0 (Transcription Factors)
RN  - 0 (enhanced green fluorescent protein)
RN  - 0 (insulin gene enhancer binding protein Isl-1)
RN  - 147336-22-9 (Green Fluorescent Proteins)
RN  - EC 2.7.7.- (Cre recombinase)
RN  - EC 2.7.7.- (Integrases)
SB  - IM
MH  - Animals
MH  - Apoptosis
MH  - Embryo, Mammalian/metabolism
MH  - Female
MH  - Green Fluorescent Proteins/genetics/metabolism
MH  - Heart/anatomy & histology/growth & development/*physiology
MH  - Homeobox Protein Nkx-2.5
MH  - Homeodomain Proteins/genetics/metabolism
MH  - Integrases/genetics/metabolism
MH  - LIM-Homeodomain Proteins/metabolism
MH  - Male
MH  - Mice
MH  - Myocytes, Cardiac/*cytology/metabolism
MH  - Phenotype
MH  - Proto-Oncogene Proteins c-myc/genetics/metabolism
MH  - Recombination, Genetic
MH  - Stem Cells/cytology/metabolism
MH  - Transcription Factors/genetics/metabolism
EDAT- 2014/09/10 06:00
MHDA- 2015/06/04 06:00
CRDT- 2014/09/10 06:00
PHST- 2014/02/05 00:00 [received]
PHST- 2014/04/21 00:00 [revised]
PHST- 2014/08/01 00:00 [accepted]
PHST- 2014/09/10 06:00 [entrez]
PHST- 2014/09/10 06:00 [pubmed]
PHST- 2015/06/04 06:00 [medline]
AID - S2211-1247(14)00668-8 [pii]
AID - 10.1016/j.celrep.2014.08.005 [doi]
PST - ppublish
SO  - Cell Rep. 2014 Sep 25;8(6):1741-1751. doi: 10.1016/j.celrep.2014.08.005. Epub 
      2014 Sep 4.