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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Fu, Xueyao Baldini, Antonio Ai, Di Lu, Mei-fang Wang, Jun Chen, Li Klein, William H. Martin, James F. |
| Description | Author Affiliation: Ai D ( Institute of Biosciences and Technology, Texas A&M System Health Science Center, 2121 Holcombe Boulevard, Houston, TX 77030, USA.); |
| Abstract | The second heart field (SHF), progenitor cells that are initially sequestered outside the heart, migrates into the heart and gives rise to endocardium, myocardium, and smooth muscle. Because of its distinct developmental history, the SHF is likely subjected to different signals from that of the first heart field. Previous experiments revealed that canonical Wnt signaling negatively regulated first heart field specification. We inactivated the obligate canonical Wnt effector beta-catenin using a beta-catenin conditional null allele and the Mef2c AHF cre driver that directs cre activity specifically in SHF. We also expressed a stabilized form of beta-catenin to model continuous Wnt signaling in SHF. Our data indicate that Wnt signaling acts in a positive fashion to promote right ventricular and interventricular myocardial expansion. Cyclin D2 and Tgfbeta2 expression was drastically reduced in beta-catenin loss-of-function mutants, indicating that Wnt signaling is required for patterning and expansion of SHF derivatives. Our findings reveal that Wnt signaling plays a major positive role in promoting growth and diversification of SHF precursors into right ventricular and interventricular myocardium. |
| ISSN | 00278424 |
| e-ISSN | 10916490 |
| Journal | Proceedings of the National Academy of Sciences of the United States of America |
| Issue Number | 22 |
| Volume Number | 104 |
| Language | English |
| Publisher | National Academy of Sciences |
| Publisher Date | 2007-05-01 |
| Publisher Place | United States |
| Access Restriction | Open |
| Subject Keyword | Heart Ventricles Embryology Metabolism Signal Transduction Wnt Proteins Animals Biological Markers Bone Morphogenetic Protein 4 Bone Morphogenetic Proteins Cell Lineage Embryo, Mammalian Cytology Gene Deletion Gene Expression Regulation, Developmental Mice Mice, Transgenic Mutation Genetics Phenotype Stem Cells Beta Catenin Deficiency Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't Multidisciplinary |
| Content Type | Text |
| Resource Type | Article |
| Subject | Multidisciplinary |
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