期刊
DEVELOPMENTAL CELL
卷 18, 期 2, 页码 275-287出版社
CELL PRESS
DOI: 10.1016/j.devcel.2010.01.008
关键词
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资金
- National Institutes for Health [R01-HL064632, R01-HL087825, U01-HL100405]
- American Heart Association Jon Holden DeHaan Foundation Myogenesis Center
- Penn Institute for Regenerative Medicine
- American Heart Association
Little is understood about the molecular mechanisms underlying the morphogenesis of the posterior pole of the heart. Here we show that Wnt2 is expressed specifically in the developing inflow tract mesoderm, which generates portions of the atria and atrioventricular canal. Loss of Wnt2 results in defective development of the posterior pole of the heart, resulting in a phenotype resembling the human congenital heart syndrome complete common atrio-ventricular canal. The number and proliferation of posterior second heart field progenitors is reduced in Wnt2(-/-) mutants. Moreover, these defects can be rescued in a temporally restricted manner through pharmacological inhibition of Gsk-3 beta. We also show that Wnt2 works in a feedforward transcriptional loop with Gata6 to regulate posterior cardiac development. These data reveal a molecular pathway regulating the posterior cardiac mesoderm and demonstrate that cardiovascular defects caused by loss of Wnt signaling can be rescued pharmacologically in vivo.
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