ArticleToxicological sciences : an official journal of the Society of Toxicology2015
The miR-322-TRAF3 circuit mediates the pro-apoptotic effect of high glucose on neural stem cells.
Article in Toxicological sciences : an official journal of the Society of Toxicology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 68 citations in OpenAlex.
- Neurotoxic Effects of Atrazine on Dopaminergic System via miRNAs and Energy-Sensing Pathways.Molecular neurobiology · 2025Article
- MiR-322-5p is involved in regulating chondrocyte proliferation and differentiation in offspring's growth plate of maternal gestational diabetes.Scientific reports · 2024Article
- MicroRNA-322 overexpression reduces neural tube defects in diabetic pregnancies.American journal of obstetrics and gynecology · 2024Article
- MicroRNA 322-5p reduced neuronal inflammation via the TLR4/TRAF6/NF-κB axis in a rat epilepsy model.Open medicine (Warsaw, Poland) · 2022Article
- TNF Signaling Acts Downstream of MiR-322/-503 in Regulating DM1 Myogenesis.Frontiers in endocrinology · 2022Article
- Nuclear factor I-C disrupts cellular homeostasis between autophagy and apoptosis via miR-200b-Ambra1 in neural tube defects.Cell death & disease · 2021Article
- Micronutrient imbalance and common phenotypes in neural tube defects.Genesis (New York, N.Y. : 2000) · 2021Review
- Maternal diabetes induces senescence and neural tube defects sensitive to the senomorphic rapamycin.Science advances · 2021Article
- Emerging roles of microRNAs in intestinal ischemia/reperfusion-induced injury: a review.Journal of physiology and biochemistry · 2020Review
- Deficiency of the oxidative stress-responsive kinase p70S6K1 restores autophagy and ameliorates neural tube defects in diabetic embryopathy.American journal of obstetrics and gynecology · 2020Article
- miR-322 treatment rescues cell apoptosis and neural tube defect formation through silencing NADPH oxidase 4.CNS neuroscience & therapeutics · 2020Article
- miR-339-3p regulated acute pancreatitis induced by caerulein through targeting TNF receptor-associated factor 3 in AR42J cells.Open life sciences · 2020Article
- The Role of MicroRNAs in Diabetes-Related Oxidative Stress.International journal of molecular sciences · 2019Review
- MicroRNA-29b-3p reduces intestinal ischaemia/reperfusion injury via targeting of TNF receptor-associated factor 3.British journal of pharmacology · 2019Article
- Downregulation of miR-322 promotes apoptosis of GC-2 cell by targeting Ddx3x.Reproductive biology and endocrinology : RB&E · 2019Article
- MiR322 mediates cardioprotection against ischemia/reperfusion injury via FBXW7/notch pathway.Journal of molecular and cellular cardiology · 2019Article
- MicroRNA-322 Regulates Self-renewal of Mouse Spermatogonial Stem Cells throughInternational journal of biological sciences · 2019Article
- High Glucose Inhibits Neural Stem Cell Differentiation Through Oxidative Stress and Endoplasmic Reticulum Stress.Stem cells and development · 2018Article
- MicroRNA-322 Cluster Promotes Tau Phosphorylation via Targeting Brain-Derived Neurotrophic Factor.Neurochemical research · 2018Article
- TRAF3 as a Multifaceted Regulator of B Lymphocyte Survival and Activation.Frontiers in immunology · 2018Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Maternal diabetes increases the risk of neural tube defects (NTDs), and caspase-dependent apoptosis and gene dysregulation are implicated in this disease process. This study investigates the role of miR-322 and its putative target gene, TNF receptor-associated factor 3 (TRAF3), in high glucose-induced apoptosis. miR-322 and TRAF3 expression were assessed in embryos of nondiabetic and diabetic dams, and in neural stem cells under high glucose conditions. Maternal diabetes in vivo and high glucose in vitro significantly down-regulated miR-322 and up-regulated TRAF3 protein expression. Overexpression of the antioxidant enzyme, superoxide dismutase 1 (SOD1), or treatment with the SOD1 mimetic Tempol, abolished the effect of maternal diabetes or high glucose on miR-322 and TRAF3 expression, respectively. A miRNA target prediction algorithm reveals 2 miR-322 binding sites the 3'-untranslated region (UTR) of TRAF3 mRNA. A RNA pull-down assay using biotin-labeled miR-322 revealed that miR-322 interacted with the 3'-UTR of TRAF3 mRNA at one specific binding site. The miR-322 mimic or TRAF3 knockdown blocked high glucose-increased TRAF3 protein expression and apoptosis, whereas the miR-322 inhibitor mimicked the effect of high glucose leading to TRAF3 up-regulation and apoptosis. This study demonstrates that both maternal diabetes and high glucose negatively regulate miR-322 through oxidative stress. miR-322 interacts with the 3'-UTR of TRAF3 and represses its translation. The miR-322-TRAF3 pathway is implicated in high glucose-induced caspase activation and apoptosis.
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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 OpenQuestion graph.