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Embryonic Heart Development (embryonic + heart_development)
Selected AbstractsThe Effect of Vascular Endothelial Growth Factor on in vitro Embryonic Heart Development in RatsANATOMIA, HISTOLOGIA, EMBRYOLOGIA, Issue 6 2004H. Ülger Summary In vitro effects of vascular endothelial growth factor (VEGF) on heart development and total embryonic growth were investigated in 84 rat embryos (obtained from nine pregnant females) at 9.5 days of gestation that were cultured in whole rat serum (WRS), in <30 kDa + >50 kDa serum fractions [retenate (R)], and in R + VEGF. After 24-h culture, the embryos from each group were harvested and divided into two groups. One group was analysed morphologically and biochemically to obtain embryo protein content, the second group was serially sectioned and examined by light microscopy. Morphological score, embryo protein content, somite number and crown-rump length of embryos indicated that embryos cultured in R had significant embryonic retardation, whereas the addition of VEGF to R increased embryonic growth and development. The morphological scores for WRS, R and R + VEGF were 57.7 ± 0.87, 46.6 ± 1.90 and 52.1 ± 0.97, somite numbers were 26.5 ± 0.47, 20.1 ± 0.63 and 24.4 ± 0.46, crown-rump lengths were 3 ± 0.07, 2.4 ± 0.06 and 2.7 ± 0.06 mm, and embryo protein contents were 160.5 ± 7.41, 98.2 ± 4.81 and 141.1 ± 10.96 ,g per embryo, respectively. The results of histological examination of heart development were similar. The hearts of embryos grown in R were unseptated and tubular. The atrioventricular endocardial cushions were incompletely developed. The addition of VEGF to R improved heart development. There were no gross morphological differences in the cardiac development between embryos grown in WRS and R + VEGF. In both groups, development of the muscular interventricular septum had begun. Development of the atrioventricular cushions was also similar in both groups and had caused narrowing of the atrioventricular canals, but the atrial septation was not observed. [source] Mechanics and function in heart morphogenesisDEVELOPMENTAL DYNAMICS, Issue 2 2005Thomas Bartman Abstract For years, biomechanical engineers have studied the physical forces involved in morphogenesis of the heart. In a parallel stream of research, molecular and developmental biologists have sought to identify the molecular pathways responsible for embryonic heart development. Recently, several studies have shown that these two avenues of research should be integrated to explain how genes expressed in the heart regulate early heart function and affect physical morphogenetic steps, as well as to conversely show how early heart function affects the expression of genes required for morphogenesis. This review combines the perspectives of biomechanical engineering and developmental biology to lay out an integrated view of the role of mechanical forces in heart development. Developmental Dynamics 233:373,381, 2005. © 2005 Wiley-Liss, Inc. [source] Regulation of dHAND protein expression by all- trans retinoic acid through ET-1/ETAR signaling in H9c2 cellsJOURNAL OF CELLULAR BIOCHEMISTRY, Issue 2 2006Weixin Li Abstract dHAND is thought to be a cardiac-restricted transcription factor during embryonic development. Vertebrate heart development involves many transcription factors such as Nkx2.5, GATA, and tbx5. All- trans retinoic acid (AtRA), the oxidative metabolite of vitamin A, can regulate the expression of these factors to affect embryonic heart development. However, the action of atRA on the expression of dHAND is rarely reported. To clarify whether atRA regulate the dHAND expression, we exposed cultured H9c2 cells (rat embryonic cardiomyocytes) to atRA and detected the protein expression of dHAND by Western blot analysis. We observed atRA can regulate the dHAND expression in a dose- and time-dependent manner. AtRA also inhibited endothelin-1 (ET-1) expression in a time-dependent manner. Further studies revealed that pretreatment with 10 µM BQ-123, a selective endothelin-1 receptor (ETAR) antagonist, for 2 h can significantly counteract the inhibition of 5 µM atRA treatment for 2 h of dHAND mRNA and protein expression. Taken together, these results suggest that atRA regulates dHAND expression by ET-1/ETAR signal transduction pathway in H9c2 cells. The mechanism of ET-1/ETAR signaling in controlling the level of dHAND protein is to reduce the levels of dHAND mRNA. It is possible for atRA to exert its cardiac teratogenesis during vertebrate embryonic development in this way. J. Cell. Biochem. 99: 478,484, 2006. © 2006 Wiley-Liss, Inc. [source] Non-invasive tracking of avian development in vivo by MRINMR IN BIOMEDICINE, Issue 4 2009Bianca Hogers Abstract Conventional microscopic techniques, to study embryonic development, require large numbers of embryos and are invasive, making follow-up impossible. We explored the use of in vivo MRI to study embryonic development, in general, and cardiovascular development in particular, over time. Wild-type quail embryos (n,=,11) were imaged at embryonic days 3, 5, 7, 9, and 11, covering the main time course of embryonic heart development. On each imaging day cardiac morphology was evaluated and embryonic length was measured. MRI-embryos as well as control embryos (n,=,11) were sacrificed at day 11 and scored for external malformations, while embryonic wet weight and stage were determined. In addition, venous clipped embryos (n,=,4), known to develop cardiovascular malformations, were scanned at regular intervals and sacrificed at day 9 for histological analysis ex vivo. We were able to follow heart development of individual quail embryos inside their shell non-invasively over time, with sufficient detail to study cardiac morphology in vivo. We did not find any adverse effect of the repeated MRI examinations on morphology, length, or weight. Prenatally diagnosed malformations, like ventricular septal defects and aortic arch interruptions were confirmed by histology. In conclusion, micro-MRI can be used to evaluate in vivo early embryonic development and to diagnose cardiovascular malformations prenatally. Copyright © 2008 John Wiley & Sons, Ltd. [source] | ||||||||||