ArticleBirth defects research2019
Embryonic cell migratory capacity is impaired upon exposure to glucose in vivo and in vitro.
Article in Birth defects research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed, 4 citations in OpenAlex.
- The Interplay Between Stiffness and Hyperglycemia on Diabetic Foot Ulcer Wound Closure.Cellular and molecular bioengineering · 2026Article
- Pathogenesis of neural tube defects: The regulation and disruption of cellular processes underlying neural tube closure.WIREs mechanisms of disease · 2022Review
- Mitochondria in Early Forebrain Development: From Neurulation to Mid-Corticogenesis.Frontiers in cell and developmental biology · 2021Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 2 countries.
Funding
Abstract
backgroundImpairments 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.
methodsWe 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.
resultsExpression 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.
conclusionsPrimary 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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.