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Experimental Study on the Effect and Mechanism of Elevated Glucose on Heart Development in Zebrafish Embryos

Author: LiangJinTao
Tutor: GuiYongHao
School: Fudan University
Course: Pediatrics
Keywords: High sugar Zebrafish Congenital heart disease tbx5 tbx20 has2 Growth retardation Original pay hybridization Development behind Cyclization barriers notch1b bmp4 IGFBP-1a
CLC: R725.4
Type: PhD thesis
Year: 2010
Downloads: 83
Quote: 0
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Abstract


The first part of the impact of high glucose on the heart development of zebrafish embryos [Objective] The pathogenesis of congenital heart disease is very complex, involving both genetic basis and non-genetic risk factors. The majority of congenital heart disease is more and more attention by the interaction between genetic and environmental factors are the formation of non-genetic risk factors for heart development. Epidemiological data indicate that: gestational diabetes mellitus (PGDM) is an important non-genetic risk factors for congenital heart disease; hyperglycemia is an the PGDM important teratogenic factor. At present, the impact of high glucose on embryonic heart development and the mechanism is unclear. In this study, the zebra fish as a model organism to study the high sugar embryonic heart development. [Method] different developmental stages (6 hpf. 24 hpf. 36 hpf) zebrafish embryos D-glucose environment respectively exposed to 12 or 24 hours, 72 hpf under a dissecting microscope counting embryonic heart malformations percentage to determine during cardiac development sugar sensitive time window. Follow-up test exposure period 6-30 hpf as separate L-glucose treated osmotic pressure control. Counting the number of somites measuring head - torso angle to determine the degree of embryonic development; cameras record cardiac phenotype changes; to cmlc2 as a cardiac marker genes through embryo whole mount in situ hybridization to determine the degree of development of the heart. [] 6-30 hpf of heart malformations period incidence highest; With the exposure start time shift, the the heart malformations proportion gradually decline. Zebrafish embryos after exposure to high glucose severe growth retardation and developmental backwardness. The heart development significantly behind, and roughly synchronized with the degree of embryonic backward. High glucose zebrafish embryos to a variety of cardiac malformations, pericardial edema, heart cyclization barriers to blood regurgitation. L-glucose had no significant effect on embryonic heart development. [Conclusion] zebrafish embryonic heart development process of high the sugar sensitive time window is 6-30 hpf, high sugar can cause heart development of zebrafish embryos backward and a variety of cardiac malformations. Caused by the second part of the high sugar zebrafish embryonic heart development backward mechanism [Objective] To explore the high sugar cause behind heart development of zebrafish embryos mechanism. [Method] in situ hybridization and qRT-PCR detected IGFBP-1a, IGFBP-1b, IGFBP-2 gene expression. [Results] caused by high sugar IGFBP-la mRNA expression in advance and increased IGFBP-1b after exposure to high glucose, IGFBP-2 expression did not change significantly. [Conclusion] IGFBP-1a expression change in high glucose caused embryonic heart development backward process. The third part caused by high glucose zebrafish embryonic heart malformations mechanism [Objective] To clarify the high sugar affect cardiac morphogenesis originating link and cause heart malformations mechanism. [Method] to nkx2.5 and cmlc2 as cardiac marker genes, early heart formation process by in situ hybridization study high glucose; situ hybridization detection tbx5, tbx20 notch1b bmp4, has2 genes in the expression of the heart. [Results] the cardiac primordia from high sugar impact heart tube cyclization is the first to be affected link. The normal control group tbx5, tbx20 embryonic heart showed ventricular advantage expression; high sugar processing the cardiac malformations embryonic tbx5 after ventricular atrium were apparent expression while tbx20 in ventricular, atrial expression significantly reduced. The normal control group notch1b, bmp4 expression confined to the atrioventricular canal endocardial layer and myocardial layer; treatment of high sugar notch 1b, bmp4 expression throughout the atrioventricular canal, there are varying degrees of expression in the ventricular zone. The normal controls has2 expression endocardial layer confined to the atrioventricular canal area, high-sugar processed has2 heart expression upregulated expression domain expanded significantly, throughout the atrioventricular canal. The earliest affected part of the process of cardiac morphogenesis [Conclusion] high glucose heart tube cyclization cyclization obstacle is the origin of cardiac abnormalities. High sugar caused the cyclization barriers tbx5, tbx20 cardiac expression related to changes; bmp4 notch lb and has2, the cardiac expression changes may be caused by high sugar heart valve abnormalities mechanism.

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CLC: > Medicine, health > Pediatrics > Children within the science > Pediatric cardiac and vascular disease
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