胚胎细胞在体内和体外暴露于葡萄糖后迁移能力受损。
Embryonic cell migratory capacity is impaired upon exposure to glucose in vivo and in vitro.
机构信息
University of Heidelberg Medical School, Heidelberg, Germany.
Department of Developmental Biology, Pennington Biomedical Research Center, Baton Rouge, Louisiana.
出版信息
Birth Defects Res. 2019 Aug 15;111(14):999-1012. doi: 10.1002/bdr2.1398. Epub 2018 Nov 19.
BACKGROUND
Impairments in cell migration during vertebrate gastrulation lead to structural birth defects, such as heart defects and neural tube defects. These defects are more frequent in progeny from diabetic pregnancies, and we have recently provided evidence that maternal diabetes leads to impaired migration of embryonic mesodermal cells in a mouse model of diabetic pregnancy.
METHODS
We here report the isolation of primary cell lines from normal and diabetes-exposed embryos of the nonobese diabetic mouse strain, and characterization of their energy metabolism and expression of nutrient transporter genes by quantitative real-time PCR.
RESULTS
Expression levels of several genes in the glucose transporter and fatty acid transporter gene families were altered in diabetes-exposed cells. Notably, primary cells from embryos with prior in vivo exposure to maternal diabetes exhibited reduced capacity for cell migration in vitro.
CONCLUSIONS
Primary cells isolated from diabetes-exposed embryos retained a "memory" of their in vivo exposure, manifesting in cell migration impairment. Thus, we have successfully established an in vitro experimental model for the mesoderm migration defects observed in diabetes-exposed mouse embryos.
背景
脊椎动物原肠胚形成过程中细胞迁移受损会导致结构出生缺陷，如心脏缺陷和神经管缺陷。这些缺陷在糖尿病孕妇的后代中更为常见，我们最近的研究证据表明，糖尿病会导致糖尿病妊娠小鼠模型中胚胎中胚层细胞迁移受损。
方法
我们在此报告了从非肥胖型糖尿病（NOD）小鼠正常和糖尿病暴露胚胎中分离原代细胞系，并通过定量实时 PCR 对其能量代谢和营养转运体基因的表达进行了表征。
结果
葡萄糖转运体和脂肪酸转运体基因家族中的几个基因的表达水平在糖尿病暴露的细胞中发生了改变。值得注意的是，先前在体内暴露于母体糖尿病的胚胎来源的原代细胞在体外的细胞迁移能力降低。
结论
从糖尿病暴露的胚胎中分离的原代细胞保留了其体内暴露的“记忆”，表现为细胞迁移受损。因此，我们成功建立了一个用于研究糖尿病暴露的小鼠胚胎中观察到的中胚层迁移缺陷的体外实验模型。
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