Document Detail


Endogenous Wnt/beta-catenin signaling is required for cardiac differentiation in human embryonic stem cells.
MedLine Citation:
PMID:  20559569     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: Wnt/beta-catenin signaling is an important regulator of differentiation and morphogenesis that can also control stem cell fates. Our group has developed an efficient protocol to generate cardiomyocytes from human embryonic stem (ES) cells via induction with activin A and BMP4. METHODOLOGY/PRINCIPAL FINDINGS: We tested the hypothesis that Wnt/beta-catenin signals control both early mesoderm induction and later cardiac differentiation in this system. Addition of exogenous Wnt3a at the time of induction enhanced cardiac differentiation, while early inhibition of endogenous Wnt/beta-catenin signaling with Dkk1 inhibited cardiac differentiation, as indicated by quantitative RT-PCR analysis for beta-myosin heavy chain (beta-MHC), cardiac troponin T (cTnT), Nkx2.5, and flow cytometry analysis for sarcomeric myosin heavy chain (sMHC). Conversely, late antagonism of endogenously produced Wnts enhanced cardiogenesis, indicating a biphasic role for the pathway in human cardiac differentiation. Using quantitative RT-PCR, we show that canonical Wnt ligand expression is induced by activin A/BMP4 treatment, and the extent of early Wnt ligand expression can predict the subsequent efficiency of cardiogenesis. Measurement of Brachyury expression showed that addition of Wnt3a enhances mesoderm induction, whereas blockade of endogenously produced Wnts markedly inhibits mesoderm formation. Finally, we show that Wnt/beta-catenin signaling is required for Smad1 activation by BMP4. CONCLUSIONS/SIGNIFICANCE: Our data indicate that induction of mesoderm and subsequent cardiac differentiation from human ES cells requires fine-tuned cross talk between activin A/BMP4 and Wnt/beta-catenin pathways. Controlling these pathways permits efficient generation of cardiomyocytes for basic studies or cardiac repair applications.
Authors:
Sharon L Paige; Tomoaki Osugi; Olga K Afanasiev; Lil Pabon; Hans Reinecke; Charles E Murry
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2010-06-15
Journal Detail:
Title:  PloS one     Volume:  5     ISSN:  1932-6203     ISO Abbreviation:  PLoS ONE     Publication Date:  2010  
Date Detail:
Created Date:  2010-06-18     Completed Date:  2010-09-01     Revised Date:  2010-09-30    
Medline Journal Info:
Nlm Unique ID:  101285081     Medline TA:  PLoS One     Country:  United States    
Other Details:
Languages:  eng     Pagination:  e11134     Citation Subset:  IM    
Affiliation:
Department of Pathology, University of Washington, Seattle, Washington, United States of America.
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MeSH Terms
Descriptor/Qualifier:
Bone Morphogenetic Protein 4 / physiology
Cell Differentiation*
Embryonic Stem Cells / metabolism*
Humans
Mesoderm / cytology
Myocardium / cytology*
Reverse Transcriptase Polymerase Chain Reaction
Signal Transduction*
Smad Proteins / metabolism
Wnt Proteins / metabolism*
beta Catenin / metabolism*
Grant Support
ID/Acronym/Agency:
F30HL095343/HL/NHLBI NIH HHS; P01 GM081719/GM/NIGMS NIH HHS; P01 HL03174/HL/NHLBI NIH HHS; R01 HL084642/HL/NHLBI NIH HHS; R01 HL64387/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Bone Morphogenetic Protein 4; 0/Smad Proteins; 0/Wnt Proteins; 0/beta Catenin
Comments/Corrections

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