Shortened outflow tract leads to altered cardiac looping after neural crest ablation

Yelbuz, T. Mesud; Waldo, Karen; Kumiski, Donna; Stadt, Harriett A.; Wolfe, Raymond R.; Leatherbury, Linda; Kirby, Margaret L.

doi:10.1016/s0735-1097(02)81833-2

Cited by 62 publications

(110 citation statements)

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“…Most recently, Waldo et al (2005a) found that neural crest (NC) cells modulate the SHF. These authors found that after experimental neural crest ablation in chicken embryos, the SHF precardiac cells failed to join the conotruncus, so the outflow tract could not elongate, remaining short, confirming then this sort of previous observation as reported by Yelbuz et al (2002). Furthermore, the same authors (Waldo et al, 2005a(Waldo et al, , 2005b found also that NC ablation did not interfere with the migration of SHF smooth muscle precursor cells to the caudal portion of the aortic sac; however, the conotruncus being short and unable to expand caudally, as a consequence even the caudal portion of the aortic sac could not expand further downward, failing then to elongate.…”

Section: Secondary Heart Fieldsupporting

confidence: 73%

“…Furthermore, most recent reports by Ward et al (2005) and Ward and Kirby (2006) emphasize the hypothesis that a short outflow tract, as obtained experimentally by them through SHF ablation and as previously obtained through experimental NC ablation (Yelbuz et al, 2002;Waldo et al, 2005a) and with consequent low SHF cellular output to the conotruncal region, does not allow a normal conotruncal rotation. Based on this hypothesis, the authors explain NC-related conotruncal heart defects such as PTA, tetralogy of Fallot (TF), pulmonary atresia with ventricular septal defect (VSD), and double-outlet right ventricle (DORV) as a consequence of the primary short conotruncal morphology.…”

Section: Secondary Heart Fieldmentioning

confidence: 76%

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Cardiac outflow tract: A review of some embryogenetic aspects of the conotruncal region of the heart

et al. 2006

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A review concerning some embryogenetic aspects of the cardiac outflow tract is presented. Two main topics are discussed: the truncal septation and the secondary heart field. In the context of the septation of the truncus arteriosus, the development of the arterial valves is largely discussed, particularly in reference to the sinuses of Valsalva. Emphasis is also given to the fate of the external myocardial wall of the truncus arteriosus, as this primordial myocardial surface disappears later in the development. Molecular genetics data concerning Sox4 and NF-Atc transcription factors are correlated in the present review with rare forms of truncus malformations encountered in human pathology. The roles exerted by the secondary heart field and the neural crest on the development and growth of the conotruncal musculature are largely discussed. Reported experimental ablations of both secondary heart field and neural crest, showed conotruncal defects such as persistent truncus arteriosus, tetralogy of Fallot, and double-outlet right ventricle, which were considered as the result of a short outflow tract causing, ultimately, a lack of conotruncal rotation. In this regard, some morphologic correlations are carried out, in the present review, between these experimental animal models and human malformations, and it is thought that this sort of conotruncal defects cannot be explained always in terms of conotruncal hypoplasia. Finally, influence of Pitx2c, a left-right laterality signaling gene, on the modulation of the conotruncal rotation, as most recently reported, is emphasized in terms of very likely multifactorial contributions in the embryogenesis of the conotruncal region of the heart. Anat Rec Part A, 288A: 936-943, 2006

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Section: Secondary Heart Fieldsupporting

confidence: 73%

Section: Secondary Heart Fieldmentioning

confidence: 76%

Cardiac outflow tract: A review of some embryogenetic aspects of the conotruncal region of the heart

et al. 2006

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“…Early alterations in looping and OFT elongation (before the neural crest is known to colonize the OFT) documented in the chick NCA model and observed in the present study are also consistent with such an indirect effect. Recent studies in the chick have shown that ablation of the cardiac neural crest results in failure of the myocardial component of the secondary heart field to migrate into the OFT (Yelbuz et al, 2002(Yelbuz et al, , 2003Waldo et al, 2005), suggesting that in addition to the direct role the cardiac neural crest plays in OFT septation, it also plays an indirect role in OFT morphogenesis by modulating secondary heart field function. Interestingly, in the present study, when partial cardiac neural crest ablation took place (two-injection group, and female embryos in three-injection group), we also observed a wide spectrum of OFT misalignment defects reminiscent of those seen when secondary heart field function is disturbed (Vitelli et al, 2002;Brown et al, 2004;Xu et al, 2004).…”

Section: Potential Nonautonomous Effects Of Ncamentioning

confidence: 99%

Temporal–spatial ablation of neural crest in the mouse results in cardiovascular defects

Porras

Brown

2007

Developmental Dynamics

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Neural crest cells are thought to play a critical role in human conotruncal morphogenesis and dysmorphogenesis. Much of our understanding of the contribution of neural crest to cardiovascular patterning comes from ablation and transplantation experiments in avian species. Although fate mapping experiments in mice suggests a conservation of function, the functional requirement for neural crest in cardiovascular development in mammals has not been formally tested. We used a novel two component genetic system for the temporal-spatial ablation of neural crest in the mouse. Affected embryos displayed a spectrum of cardiovascular outflow tract defects and aortic arch patterning abnormalities. We show that the severity of the cardiovascular phenotype is directly related to the level and extent of neural crest ablation. This is the first report of cardiac neural crest ablation in mammals, and it provides important insight into the role of the mammalian neural crest during cardiovascular development. Developmental Dynamics 237:153-162, 2008.

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“…Studies have found that impaired folate and homocystiene metabolism affects neural crest cells formation and migration leading to defect in trunco-conal septum and mal alignment of outflow tract, resulting in CTDs [25]. Since MTHFR polymorphism affects folate and homocystiene metabolism, the presence of such polymorphism can result in impaired folate metabolism, and a resultant defect in neural crest cell formation and migration, and subsequent CTD formation.…”

Section: Discussionmentioning

confidence: 99%

Genetic Variants in the Methylenetetrahydrofolate Reductase Gene in Egyptian Children with Conotruncal Heart Defects and their Mothers

Kotby

Anwar

Elmasry

et al. 2012

Macedonian Journal of Medical Sciences

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Aim: This study aimed at evaluation of MTHFR 677C/T and 1298A/C polymorphisms in MTHFR gene as maternal risk factors in conotruncal heart defects (CTDs). Material and Methods:Thirty cases with CTDs and their mothers and thirty control children and their mothers were studied. Medical and nutritional histories for all mothers were taken with emphasis on folate intake. The mutations in MTHFR gene are a C to T substitution at base pair 677 and a A to C at base pair1298 were investigated by polymerase-chain reaction, followed by restriction enzyme digestion and detection by electrophoresis.Results: Folic acid intake was below the recommended daily allowance in case mothers compared to control mothers. No significant difference between patients and control group or their mothers regarding MTHFR gene polymorphisms at exon 4. Significant difference between case and control groups and between their mothers regarding MTHFR gene polymorphisms at exon 7. Homozygous genotype frequencies of MTHFR at position 1298 was significantly higher in cases and their mothers with an odds ratio 56 (95% confidence interval 10.3-303.7).Conclusion: Egyptian population may have high incidence of MTHFR polymorphism at exon 7 rather than at exon 4. Preconception folate intake might decrease MTHFR polymorphism at exon 7 and decrease risk of CTD.

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Shortened outflow tract leads to altered cardiac looping after neural crest ablation

Cited by 62 publications

References 0 publications

Cardiac outflow tract: A review of some embryogenetic aspects of the conotruncal region of the heart

Cardiac outflow tract: A review of some embryogenetic aspects of the conotruncal region of the heart

Temporal–spatial ablation of neural crest in the mouse results in cardiovascular defects

Genetic Variants in the Methylenetetrahydrofolate Reductase Gene in Egyptian Children with Conotruncal Heart Defects and their Mothers

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