Transient increase in VEGF-A leads to cardiac tube anomalies and increased risk of congenital heart malformations
| Autor: | Sandra Rugonyi, Graham Rykiel, Brenda J. Rongish, Mackenzie J. Gray |
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| Rok vydání: | 2021 |
| Předmět: |
0301 basic medicine
Heart Defects Congenital Vascular Endothelial Growth Factor A medicine.medical_specialty Histology Heart malformation 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Internal medicine biology.animal medicine Morphogenesis Humans Ecology Evolution Behavior and Systematics biology Tubular heart Heart development business.industry Myocardium Embryogenesis Infant Newborn Embryo Heart Quail Vascular endothelial growth factor 030104 developmental biology chemistry In utero Cardiology Female Anatomy business 030217 neurology & neurosurgery Biotechnology |
| Zdroj: | Anatomical record (Hoboken, N.J. : 2007)REFERENCES. 304(12) |
| ISSN: | 1932-8494 |
| Popis: | Vascular endothelial growth factor (VEGF) plays a critical role during early heart development. Clinical evidence shows that conditions associated with changes in VEGF signaling in utero are correlated with an increased risk of congenital heart defects (CHD) in newborns. However, how malformations develop after abnormal VEGF exposure is unknown. During embryogenesis, a primitive heart, consisting of an endocardial tube enveloped by a myocardial mantle, is the first organ to function. This tubular heart ultimately transforms into a four-chambered heart. To determine how a transient increase in VEGF prior to heart tube formation affects heart development leading to CHD, we applied exogenous VEGF or a control (vehicle) solution to quail embryos in ovo at Hamburger-Hamilton (HH) stage 8 (28-30 hr of incubation), right before heart tube formation. Light microscopy analysis of embryos re-incubated after treatment for 13 hrs (to approximately HH11/HH12) showed that increased VEGF leads to impaired heart tube elongation accompanied by diameter expansion. Micro-CT analysis of embryos re-incubated for 9 days (to approximately HH38), when the heart is fully formed, showed that VEGF treatment increased the rate of cardiac malformations in surviving embryos. Despite no sex differences in survival, female embryos were more likely to develop cardiac malformations. Our results further suggest that heart tube malformations after a transient increase in VEGF right before heart tube formation may be reversible, leading to normal hearts. |
| Databáze: | OpenAIRE |
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