Document Detail


Spontaneously beating cardiomyocytes derived from white mature adipocytes.
MedLine Citation:
PMID:  19643806     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
AIMS: Adipose stromal cells and dissociated brown adipose tissue have been shown to generate cardiomyocyte-like cells. However, it is not clear whether white mature adipocytes have the same potential, even though a close relationship has been found between adipocytes and vascular endothelial cells, another cardiovascular cell type. The objective of this study was to examine if white adipocytes would be able to supply cardiomyocytes.
METHODS AND RESULTS: We prepared a highly purified population of lipid-filled adipocytes from mice, 6-7 weeks of age. When allowed to lose lipids, the adipocytes assumed a fibroblast-like morphology, so-called dedifferentiated fat (DFAT) cells. Subsequently, 10-15% of the DFAT cells spontaneously differentiated into cardiomyocyte-like cells, in which the cardiomyocyte phenotype was identified by morphological observations, expression of cardiomyocyte-specific markers, and immunocytochemical staining. In addition, electrophysiological studies revealed pacemaker activity in these cells, and functional studies showed that a beta-adrenergic agonist stimulated the beating rate, whereas a beta-antagonist reduced it. In vitro treatment of newly isolated adipocytes or DFAT cells with inhibitors of bone morphogenetic proteins (BMP) and Wnt signalling promoted the development of the cardiomyocyte phenotype as determined by the number or beating colonies of cardiomyocyte-like cells and expression of troponin I, a cardiomyocyte-specific marker. Inhibition of BMP was most effective in promoting the cardiomyocyte phenotype in adipocytes, whereas Wnt-inhibition was most effective in DFAT cells.
CONCLUSION: White mature adipocytes can differentiate into cardiomyocyte-like cells, suggesting a link between adipocyte and cardiomyocyte differentiation.
Authors:
Medet Jumabay; Rui Zhang; Yucheng Yao; Joshua I Goldhaber; Kristina I Boström
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Cardiovascular research     Volume:  85     ISSN:  1755-3245     ISO Abbreviation:  Cardiovasc. Res.     Publication Date:  2010 Jan 
Date Detail:
Created Date:  2009-12-16     Completed Date:  2010-02-19     Revised Date:  2011-10-26    
Medline Journal Info:
Nlm Unique ID:  0077427     Medline TA:  Cardiovasc Res     Country:  England    
Other Details:
Languages:  eng     Pagination:  17-27     Citation Subset:  IM    
Affiliation:
David Geffen School of Medicine at UCLA, Los Angeles, CA 90095-1679, USA.
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MeSH Terms
Descriptor/Qualifier:
Action Potentials
Adipocytes, White / cytology*
Animals
Bone Morphogenetic Proteins / antagonists & inhibitors,  physiology
Calcium / metabolism
Cell Differentiation
Cells, Cultured
GATA4 Transcription Factor / analysis
Mice
Mice, Inbred C57BL
Myocardial Contraction
Myocytes, Cardiac / cytology*
Phenotype
Signal Transduction
Stem Cells / cytology
Wnt Proteins / antagonists & inhibitors,  physiology
Grant Support
ID/Acronym/Agency:
HL30568/HL/NHLBI NIH HHS; HL70828/HL/NHLBI NIH HHS; HL81397/HL/NHLBI NIH HHS; R01 HL070828-08/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Bone Morphogenetic Proteins; 0/GATA4 Transcription Factor; 0/Gata4 protein, mouse; 0/Wnt Proteins; 7440-70-2/Calcium
Comments/Corrections
Comment In:
Cardiovasc Res. 2010 Jan 1;85(1):1-2   [PMID:  19887381 ]

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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