ArticleBirth defects research2018
Network correlation analysis revealed potential new mechanisms for neural tube defects beyond folic acid.
Article in Birth defects research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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
1 citing paper in PubMed, 4 citations in OpenAlex.
- Competing Endogenous RNAs Crosstalk in Hippocampus: A Potential Mechanism for Neuronal Developing Defects in Down Syndrome.Journal of molecular neuroscience : MN · 2024Article
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundNeural tube defects (NTDs) are clinically significant congenital malformations which are known to be folic acid (FA) responsive, such that supplementation significantly reduces the prevalence of NTDs. Nonetheless, some individuals fail to respond to FA supplementation; hence NTDs remain a significant public health concern. The mechanisms that underlie the beneficial effects of FA supplementation remain poorly understood. Mouse models have been used extensively to study the mechanisms driving neural tube closure (NTC).
methodsMicroarray data of GSE51285 was downloaded from the NCBI GEO database, which contains the RNA expression profiles of livers from five NTD mouse mutants (heterozygous females) and their corresponding wildtype (WT) controls. Those five NTD mutants have different responsiveness to FA supplementation. The differentially expressed genes (DEGs) between NTD heterozygous and WT mice, as well as the DEGs between FA-responsive and FA-resistant mutants were carefully examined. Weighted gene correlation network analysis (WGCNA) was performed in order to identify genes with high correlations to either FA responsiveness or NTDs, respectively.
resultsIn total, we identified 18 genes related to the pathogenesis of NTDs, as well as 55 genes related to FA responsiveness. Eight more candidate genes (Abcc3, Gsr, Gclc, Mthfd1, Gart, Bche, Slc25a32, and Slc44a2) were identified by examining the DEGs of those genes involved in the extended folate metabolic pathway between FA-responsive and FA-resistant mutants.
conclusionsThose genes are involved in mitochondrial choline metabolism, de novo purine synthesis, and glutathione generation, suggesting that formate, choline, and manipulating antioxidant levels may be effective interventions in FA-resistant NTDs.
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