ArticleNutrition & metabolism2016
The effect of inhibiting glycinamide ribonucleotide formyl transferase on the development of neural tube in mice.
Article in Nutrition & metabolism, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Inhibition of Purine Metabolism Promotes the Differentiation of Neuroblastoma Driven by MYCN.Cancer medicine · 2025Article
- Fundamental origins of neural tube defects with a basis in genetics and nutrition.Experimental brain research · 2025Review
- Purinosomes and Purine Metabolism in Mammalian Neural Development: A Review.Acta histochemica et cytochemica · 2024Review
- Deletion of the neural tube defect-associated geneThe Journal of biological chemistry · 2018Article
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Authors and funding
8 authors.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundFolate deficiency is closely related to the development of neural tube defects (NTDs). However, the exact mechanism is not completely understood. This study aims to induce murine NTDs by inhibiting one of the folate metabolic pathways, de novo purine synthesis and preliminarily investigate the potential mechanisms. The key enzyme, glycinamide ribonucleotide formyl transferase (GARFT) was inhibited by a specific inhibitor, lometrexol (DDATHF) in the pregnant mice.
methodsPregnant mice were intraperitoneally injected with various doses of DDATHF on gestational day 7.5 and embryos were examined for the presence of NTDs on gestational day 11.5. GARFT activity and levels of ATP, GTP, dATP and dGTP were detected in embryonic brain tissue. Proliferation and apoptosis was analyzed by real-time quantitative polymerase chain reaction (RT-qPCR), immunohistochemical assay and western blotting.
results40 mg kg(-1) body weight (b/w) of DDATHF caused the highest incidence of NTDs (30.8 %) and therefore was selected as the optimal dose to establish murine NTDs. The GARFT activity and levels of ATP, GTP, dATP and dGTP in embryonic brain tissue were significantly decreased after DDATHF treatment. Furthermore, Levels of proliferation-related genes (Pcna, Foxg1 and Ptch1) were downregulated and apoptosis-related genes (Bax, Casp8 and Casp9) were upregulated. Expression of phosphohistone H3 was significantly decreased while expression of cleaved caspase-3 was greatly increased.
conclusionsResults indicate that DDATHF induced murine NTDs by disturbing purine metabolism and further led to abnormal proliferation and apoptosis.
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