ArticleDisease models & mechanisms2016
A new gestational diabetes mellitus model: hyperglycemia-induced eye malformation via inhibition of Pax6 in the chick embryo.
Article in Disease models & mechanisms, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 18 citations in OpenAlex.
- Distinct cellular localization of α- synuclein and β-synuclein in the chick retina.Brain structure & function · 2025Article
- Ocular Microvascular Changes in Offspring Born to Mothers With Gestational Diabetes Mellitus: The Nanjing Eye Study.Translational vision science & technology · 2025Article
- Early exposure to Western Diet exacerbates visual outcomes in female mice.bioRxiv : the preprint server for biology · 2024Article
- Chemical signaling in the developing avian retina: Focus on cyclic AMP and AKT-dependent pathways.Frontiers in cell and developmental biology · 2022Review
- Association of maternal diabetes during pregnancy with high refractive error in offspring: a nationwide population-based cohort study.Diabetologia · 2021Article
- Ophthalmic Pathology in the Offspring of Pregnant Women with Gestational Diabetes Mellitus.Maternal and child health journal · 2020Observational
- The retinal pigment epithelial response after retinal laser photocoagulation in diabetic mice.Lasers in medical science · 2019Article
- Level of hydrogen peroxide affects expression and sub-cellular localization of Pax6.Molecular biology reports · 2018Article
- The chick eye in vision research: An excellent model for the study of ocular disease.Progress in retinal and eye research · 2017Review
- PDX1 Methylation, NGN3 and Pax6 Expression Levels in Pregnant Women with Gestational Diabetes Mellitus and their association with neonatal blood sugars and birth weight.Pakistan journal of medical sciencesArticle
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gestational diabetes mellitus (GDM) is one of the leading causes of fetal malformations. However, few models have been developed to study the underlying mechanisms of GDM-induced fetal eye malformation. In this study, a high concentration of glucose (0.2 mmol per egg) was injected into the air sac of chick embryos on embryo development day (EDD) 1 to develop a hyperglycemia model. Results showed that 47.3% of embryonic eye malformation happened on EDD 5. In this model, the key genes regulating eye development, Pax6, Six3 and Otx2, were downregulated by hyperglycemia. Among these genes, the expression of Pax6 was the most vulnerable to hyperglycemia, being suppressed by 70%. A reduction in Pax6 gene expression induced eye malformation in chick embryos. However, increased expression of Pax6 in chick embryos could rescue hyperglycemia-induced eye malformation. Hyperglycemia stimulated O-linked N-acetylglucosaminylation, which caused oxidative stress in chick embryos. Pax6 was found to be vulnerable to free radicals, but the antioxidant edaravone could restore Pax6 expression and reverse eye malformation. These results illustrated a successful establishment of a new chick embryo model to study the molecular mechanism of hyperglycemia-induced eye malformation. The suppression of the Pax6 gene is probably mediated by oxidative stress and could be a crucial target for the therapy of GDM-induced embryonic eye malformation.
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