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Wnt2 coordinates the commitment of mesoderm to hematopoietic, endothelial, and cardiac lineages in embryoid bodies.

Wnt2 coordinates the commitment of mesoderm to hematopoietic, endothelial, and cardiac lineages in embryoid bodies. Research Abstract Details 

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  • Wnt2 coordinates the commitment of mesoderm to hematopoietic, endothelial, and cardiac lineages in embryoid bodies. Abstract Text:

    hong wangHong Wang,jennifer b gilnerJennifer B Gilner,victoria l bautchVictoria L Bautch,da-zhi wangDa-Zhi Wang,brandon j wainwrightBrandon J Wainwright,suzanne l kirbySuzanne L Kirby,cam pattersonCam Patterson,

    Our recent gene expression profiling analyses demonstrated that Wnt2 is highly expressed in Flk1(+) cells, which serve as common progenitors of endothelial cells, blood cells, and mural cells. In this report, we characterize the role of Wnt2 in mesoderm development during embryonic stem (ES) cell differentiation by creating ES cell lines in which Wnt2 was deleted. Wnt2(-/-) embryoid bodies (EBs) generated increased numbers of Flk1(+) cells and blast colony-forming cells compared with wild-type EBs, and had higher Flk1 expression at comparable stages of differentiation. Although Flk1(+) cells were increased, we found that endothelial cell and terminal cardiomyocyte differentiation was impaired, but hematopoietic cell differentiation was enhanced and smooth muscle cell differentiation was unchanged in Wnt2(-/-) EBs. Later stage Wnt2(-/-) EBs had either lower or undetectable expression of endothelial and cardiac genes compared with wild-type EBs. Consistently, vascular plexi were poorly formed and neither beating cardiomyocytes nor alpha-actinin-staining cells were detectable in later stage Wnt2(-/-) EBs. In contrast, hematopoietic cell gene expression was upregulated, and the number of hematopoietic progenitor colonies was significantly enhanced in Wnt2(-/-) EBs. Our data indicate that Wnt2 functions at multiple stages of development during ES cell differentiation and during the commitment and diversification of mesoderm: as a negative regulator for hemangioblast differentiation and hematopoiesis but alternatively as a positive regulator for endothelial and terminal cardiomyocyte differentiation.

    Wnt2 coordinates the commitment of mesoderm to hematopoietic, endothelial, and cardiac lineages in embryoid bodies. Publishing Authors By Initials

    h wangH Wang,jb gilnerJB Gilner,vl bautchVL Bautch,dz wangDZ Wang,bj wainwrightBJ Wainwright,sl kirbySL Kirby,c pattersonC Patterson,

    For similar peptides: intercellular signaling peptides and proteins: wnt proteins research abstracts see: peptides: intercellular signaling peptides and proteins: wnt proteins research

    PUBMED ID PMID:

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    Wnt2 coordinates the commitment of mesoderm to hematopoietic, endothelial, and cardiac lineages in embryoid bodies. Journal Published:

    PUBLICATION TYPE: Research Support, N.I.H., Extr

    Journal: The Journal of biological chemistry

    VOLUME: 282

    Page Numbers: 782-91

    Journal Abbreviation: J. Biol. Chem.

    ISSN: 0021-9258

    DAY: 10

    MONTH: 11

    YEAR: 2006

    Wnt2 coordinates the commitment of mesoderm to hematopoietic, endothelial, and cardiac lineages in embryoid bodies. Information

    Number of References:

    LANGUAGE: eng

    NlmUniqueID: 2985121

    Wnt2 coordinates the commitment of mesoderm to hematopoietic, endothelial, and cardiac lineages in embryoid bodies. Keywords Mesh Terms:

    KEYWORDS: Wnt Proteins

    MESH TERMS: physiology

    Chemical & Substance for Abstract: Wnt2 coordinates the commitment of mesoderm to hematopoietic, endothelial, and cardiac lineages in embryoid bodies. Information

    Substance Name: Wnt2b protein, mouse

    Registry Number: 0

    Grant and Affiliation Information for Wnt2 coordinates the commitment of mesoderm to hematopoietic, endothelial, and cardiac lineages in embryoid bodies.

    AFFILIATION: Carolina Cardiovascular Biology Center and Department of Medicine, University of North Carolina, Chapel Hill, North Carolina 27599, USA.

    Country: United States

    United States Research PublicationUnited States Research Publication

    AGENCY: United States NHLBI

    GRANT: HL 61656

    ACRONYM: HL

    MEDLINETA: J Biol Chem

    REFSOURCE:

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    Number Hits: 0

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