The TGFβ type II receptor plays a critical role in the endothelial cells during cardiac development

TGFβ signalling is required for normal cardiac development. To investigate which cell types are involved, we used mice carrying a floxed Type II TGFβ receptor (Tgfbr2fl) allele and Cre‐lox genetics to deplete this receptor in different regions of the heart. The three target tissues and corresponding...

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Bibliographic Details
Published in:Developmental dynamics 2010-09, Vol.239 (9), p.2435-2442
Main Authors: Robson, Andrew, Allinson, Kathleen R., Anderson, Robert H., Henderson, Deborah J., Arthur, Helen M.
Format: Article
Language:English
Subjects:
Animals
cardiogenesis
Embryo, Mammalian - anatomy & histology
Embryo, Mammalian - physiology
embryonic development
Endothelial Cells - cytology
Endothelial Cells - metabolism
Female
Heart - embryology
Heart - growth & development
Mice
Mice, Transgenic
Myocardium - cytology
Myocardium - metabolism
Pregnancy
Protein-Serine-Threonine Kinases - genetics
Protein-Serine-Threonine Kinases - metabolism
Receptors, Transforming Growth Factor beta - genetics
Receptors, Transforming Growth Factor beta - metabolism
Transforming Growth Factor beta - metabolism
ventricular septal defect
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Summary:TGFβ signalling is required for normal cardiac development. To investigate which cell types are involved, we used mice carrying a floxed Type II TGFβ receptor (Tgfbr2fl) allele and Cre‐lox genetics to deplete this receptor in different regions of the heart. The three target tissues and corresponding Cre transgenic lines were atrioventricular myocardium (using cGata6‐Cre), ventricular myocardium (using Mlc2v‐Cre), and vascular endothelium (using tamoxifen‐activated Cdh5(PAC)‐CreERT2). Spatio‐temporal Cre activity in each case was tracked via lacZ activation from the Rosa26R locus. Atrioventricular‐myocardial‐specific Tgfbr2 knockout (KO) embryos had short septal leaflets of the tricuspid valve, whereas ventricular myocardial‐specific KO embryos mainly exhibited a normal cardiac phenotype. Inactivation of Tgfbr2 in endothelial cells from E11.5 resulted in deficient ventricular septation, accompanied by haemorrhage from cerebral blood vessels. We conclude that TGFβ signalling through the Tgfbr2 receptor, in endothelial cells, plays an important role in cardiac development, and is essential for cerebral vascular integrity. Developmental Dynamics 239:2435–2442, 2010. © 2010 Wiley‐Liss, Inc.
ISSN:1058-8388
1097-0177
DOI:10.1002/dvdy.22376