• Corpus ID: 16146162

Double-Outlet Right Ventricle and Overriding Tricuspid Valve Reflect Disturbances of Looping, Myocardialization, Endocardial Cushion Differentiation, and Apoptosis in TGF-b2–Knockout Mice

@inproceedings{Bartram2001DoubleOutletRV,
  title={Double-Outlet Right Ventricle and Overriding Tricuspid Valve Reflect Disturbances of Looping, Myocardialization, Endocardial Cushion Differentiation, and Apoptosis in TGF-b2–Knockout Mice},
  author={Ulrike Bartram and Dani{\"e}l G M Molin and Lambertus J. Wisse and Azhar Mohamad and L. Philip Sanford and Thomas C. Doetschman and Christian Paul Speer and Robert E. Poelmann and Adriana C. Gittenberger-de Groot},
  year={2001}
}
Background—Transforming growth factorb2 (TGF-b2) is a member of a family of growth factors with the potential to modify multiple processes. Mice deficient in the TGFb2 gene die around birth and show a variety of defects of different organs, including the heart. Methods and Results —We studied the hearts of TGFb2–null mouse embryos from 11.5 to 18.5 days of gestation to analyze the types of defects and determine which processes of cardiac morphogenesis are affected by the absence of TGF-b2… 

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References

SHOWING 1-10 OF 35 REFERENCES
Developmental remodeling and shortening of the cardiac outflow tract involves myocyte programmed cell death.
TLDR
The results suggest that the elimination of myocytes by programmed cell death is one mechanism by which the outflow tract myocardium remodels to form the proper connection between the ventricular chambers and the appropriate arterial trunks.
RXR alpha deficiency confers genetic susceptibility for aortic sac, conotruncal, atrioventricular cushion, and ventricular muscle defects in mice.
TLDR
The intermediate phenotype of RXRalpha heterozygous embryos documents a gene dosage effect for RXR alpha in maintaining normal cardiac morphogenesis, and some defects in RXRAlpha mutant mice are phenocopies of human congenital heart defects, thereby suggesting that a relative deficiency in RXS alpha or molecules downstream in its signaling pathway may represent congenitalHeart disease-susceptibility genes.
A subpopulation of apoptosis-prone cardiac neural crest cells targets to the venous pole: multiple functions in heart development?
TLDR
Because of the perfect timing of the arrival of crest cells, their apoptosis, and a change in electrophysiological behavior of the heart, it is postulate that neural crest cells play a role in the last phase of differentiation of the cardiac conduction system.
TGF β 2 knockout mice have multiple developmental defects that are non-overlapping with other TGF β knockout phenotypes
TLDR
Targeted disruption of the TGF β 2 gene was undertaken to determine its essential role in vivo to exhibit perinatal mortality and a wide range of developmental defects for a single gene disruption.
Unilateral vitelline vein ligation alters intracardiac blood flow patterns and morphogenesis in the chick embryo.
TLDR
It is concluded that abnormal intracARDiac blood flow, resulting from hampered venous inflow, may result in serious intracardiac and pharyngeal arch artery malformations comparable to defects observed in embryonic chicken models subjected to neural crest ablation, cervical flexure experiments, and excessive retinoic acid treatment.
Requirement of type III TGF-beta receptor for endocardial cell transformation in the heart.
TLDR
A model where TBRIII localizes transformation in the heart and plays an essential, nonredundant role in TGF-beta signaling is supported.
Stereological study of stage 34 chicken hearts with looping disturbances after retinoic acid treatment: Disturbed growth of myocardium and atrioventricular cushion tissue
TLDR
The myocardial volume was hypothesized to be altered because of a decrease in contraction force of these hearts, and retinoic acid has been suggested to influence endocardial cushion volumes.
Transforming growth factor-beta in cardiac ontogeny and adaptation.
TLDR
A truncated form of the type II TGF-beta receptor, created by deletion of the cytoplasmic kinase domain, acts as a dominant suppressor of T GF-beta signal transduction in cultured cardiac muscle cells and may provide a suitable means to establish the functions of TDF-beta in vivo.
Neural crest cells in outflow tract septation of the embryonic chicken heart: Differentiation and apoptosis
TLDR
This work has studied the role of the neural crest in remodeling the outflow tract by long‐term cell tracing, differentiation markers and apoptosis, and the differentiation pathway and fate of the Neural crest cells in the out flow tract have been followed over a prolonged period.
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