Hartman Institute for Therapeutic Organ Regeneration

Bmp2 and Gata4 function additively to rescue heart tube development in the absence of retinoids.

TitleBmp2 and Gata4 function additively to rescue heart tube development in the absence of retinoids.
Publication TypeJournal Article
Year of Publication2006
AuthorsGhatpande S, Brand T, Zile M, Evans T
JournalDev Dyn
Volume235
Issue8
Pagination2030-9
Date Published2006 Aug
ISSN1058-8388
KeywordsAnimals, Apoptosis, Bone Morphogenetic Protein 2, Bone Morphogenetic Proteins, Cells, Cultured, Embryo, Nonmammalian, Endoderm, GATA4 Transcription Factor, Gene Expression Regulation, Developmental, Heart, Myocardium, Quail, Retinoids, Transcription, Genetic, Transforming Growth Factor beta, Vitamin A Deficiency
Abstract

We used the vitamin A-deficient (VAD) quail model to investigate the retinoid-dependent mechanism that regulates heart tube development. We showed previously that decreased levels of Gata4 in cardiogenic mesoderm and endoderm correlate with the cardiomyopathy caused by VAD, but that this could be rescued by transplanting normal anterior endoderm. Bmp2 is a known cardiogenic factor that is expressed normally in lateral plate mesoderm and cardiac-associated pharyngeal endoderm. Here we show that (like Gata4) transcripts encoding Bmp2 and BMP-dependent signaling activity are decreased throughout the heart-forming region of the VAD embryo. Addition of Bmp2 protein or forced expression of Gata4 in cultured VAD embryos leads to a partial rescue of the cardiomyopathy, and addition of both Bmp2 and Gata4 has an additive positive effect. Our data are consistent with a requirement for retinoid signaling to maintain expression of Bmp2, which regulates Gata4, and in addition acts with Gata4 to regulate genes important for normal morphogenesis of the primitive heart tube.

DOI10.1002/dvdy.20836
Alternate JournalDev Dyn
PubMed ID16691562
Grant ListHL61982 / HL / NHLBI NIH HHS / United States
HL64282 / HL / NHLBI NIH HHS / United States

Weill Cornell Medicine
Hartman Institute for Therapeutic Organ Regeneration
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