ArticleJournal of neuroinflammation2024
Tet1-mediated 5hmC regulates hippocampal neuroinflammation via wnt signaling as a novel mechanism in obstructive sleep apnoea leads to cognitive deficit.
Article in Journal of neuroinflammation, 2024. 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.
- Astrocytic Redox Homeostasis as a Metabolic Modulator of DNA Damage and Repair in the Ischemic Penumbra.Cells · 2026Review
- Microglia Mitochondrial Metabolism in Neurological Diseases.Molecular neurobiology · 2026Review
- From molecular damage to regulatory constraint: epigenetic and metabolic limits of cellular plasticity in aging.Frontiers in aging · 2026Review
- TET1-Mediated DNA hydroxymethylation of KLF6 promotes LPS-induced pulmonary fibrosis by activating the S1PR3/RhoA/ROCK signaling pathway.Respiratory research · 2025Article
- Subjective sleep characteristics in non-demented adults: domain-specific associations with multimodal Alzheimer's disease biomarkers.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- A ternary-code DNA methylome atlas of mouse tissues.Genome biology · 2025Article
- Relationship between Serum Neurotransmitters and Cognitive Impairment in Adults with Obstructive Sleep Apnea.Nature and science of sleep · 2025Article
- Differential expression and correlation analysis of global transcriptome for obstructive sleep apnea hypopnea syndrome.Frontiers in molecular biosciences · 2025Article
- Inflammation in Obstructive Sleep Apnea: A Global Bibliometric Perspective.Nature and science of sleep · 2025Article
- Impact of Chronic Intermittent Hypoxia on Cognitive Function and Hippocampal Neurons in Mice: A Study of Inflammatory and Oxidative Stress Pathways.Nature and science of sleep · 2024Article
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Authors and funding
8 authors.
Funding
Abstract
backgroundObstructive sleep apnoea (OSA) is a sleep-disordered breathing characterized by intermittent hypoxia (IH) that may cause cognitive dysfunction. However, the impact of IH on molecular processes involved in cognitive function remains unclear.
methodsC57BL / 6 J mice were exposed to either normoxia (control) or IH for 6 weeks. DNA hydroxymethylation was quantified by hydroxymethylated DNA immunoprecipitation (hMeDIP) sequencing. ten-eleven translocation 1 (Tet1) was knocked down by lentivirus. Specifically, cognitive function was assessed by behavioral experiments, pathological features were assessed by HE staining, the hippocampal DNA hydroxymethylation was examined by DNA dot blot and immunohistochemical staining, while the Wnt signaling pathway and its downstream effects were studied using qRT-PCR, immunofluorescence staining, and Luminex liquid suspension chip analysis.
resultsIH mice showed pathological changes and cognitive dysfunction in the hippocampus. Compared with the control group, IH mice exhibited global DNA hydroxylmethylation in the hippocampus, and the expression of three hydroxylmethylases increased significantly. The Wnt signaling pathway was activated, and the mRNA and 5hmC levels of Wnt3a, Ccnd2, and Prickle2 were significantly up-regulated. Further caused downstream neurogenesis abnormalities and neuroinflammatory activation, manifested as increased expression of IBA1 (a marker of microglia), GFAP (a marker of astrocytes), and DCX (a marker of immature neurons), as well as a range of inflammatory cytokines (e.g. TNFa, IL3, IL9, and IL17A). After Tet1 knocked down, the above indicators return to normal.
conclusionActivation of Wnt signaling pathway by hippocampal Tet1 is associated with cognitive dysfunction induced by IH.
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