ArticleMolecular medicine (Cambridge, Mass.)2020
Increased H3K4me3 methylation and decreased miR-7113-5p expression lead to enhanced Wnt/β-catenin signaling in immune cells from PTSD patients leading to inflammatory phenotype.
Article in Molecular medicine (Cambridge, Mass.), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 28 citations in OpenAlex.
- Silent regulators of trauma: the microRNA blueprint underlying post-traumatic stress disorder biology.Environmental epigenetics · 2026Review
- Loss of KDM5A-mediated H3K4me3 demethylation promotes aberrant neural development by Wnt/β-catenin pathway activation.Cell death & disease · 2025Article
- Profiling fear-extinction learning induced small ncRNAs landscape and identifying miR-29b-3p as a promising biomarker for PTSD.Journal of translational medicine · 2025Article
- The Role of Extracellular Vesicles in Neuropsychiatric Disorders.Advanced pharmaceutical bulletin · 2025Review
- Therapeutic potentials of natural products for post-traumatic stress disorder: A focus on epigenetics.Chinese herbal medicines · 2025Review
- Mapping the epigenomic landscape of post-traumatic stress disorder in human cortical neurons.medRxiv : the preprint server for health sciences · 2024Article
- Mechanism and application of feedback loops formed by mechanotransduction and histone modifications.Genes & diseases · 2024Review
- Wnt10b knockdown regulates the relative balance of adipose tissue-resident T cells and inhibits white fat deposition.Molecular biology reports · 2024Article
- Epigenetics of Fear, Anxiety and Stress - Focus on Histone Modifications.Current neuropharmacology · 2024Article
- Recent advances in the role of miRNAs in post-traumatic stress disorder and traumatic brain injury.Molecular psychiatry · 2023Review
- Review
- The neural circuits and molecular mechanisms underlying fear dysregulation in posttraumatic stress disorder.Frontiers in neuroscience · 2023Review
- The role of WNT10B in physiology and disease: A 10-year update.Frontiers in cell and developmental biology · 2023Review
- 2,3,7,8-Tetrachlorodibenzo-p-dioxin induces multigenerational alterations in the expression of microRNA in the thymus through epigenetic modifications.PNAS nexus · 2023Article
- Long non-coding RNA LINC00926 regulates WNT10B signaling pathway thereby altering inflammatory gene expression in PTSD.Translational psychiatry · 2022Article
- Central and Peripheral Immune Dysregulation in Posttraumatic Stress Disorder: Convergent Multi-Omics Evidence.Biomedicines · 2022Review
- Characterization of Altered Gene Expression and Histone Methylation in Peripheral Blood Mononuclear Cells Regulating Inflammation in COVID-19 Patients.Journal of immunology (Baltimore, Md. : 1950) · 2022Article
- MicroRNAs as biomarker and novel therapeutic target for posttraumatic stress disorder in Veterans.Psychiatry research · 2021Review
- Exosomes and Micro-RNAs in Aging Process.Biomedicines · 2021Review
- Exploring the Genetic Association of the ABAT Gene with Alzheimer's Disease.Molecular neurobiology · 2021Article
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Authors and funding
9 authors at 5 institutions in 1 country.
Funding
Abstract
backgroundPosttraumatic stress disorder (PTSD) is a psychiatric disorder accompanied by chronic peripheral inflammation. What triggers inflammation in PTSD is currently unclear. In the present study, we identified potential defects in signaling pathways in peripheral blood mononuclear cells (PBMCs) from individuals with PTSD.
methodsRNAseq (5 samples each for controls and PTSD), ChIPseq (5 samples each) and miRNA array (6 samples each) were used in combination with bioinformatics tools to identify dysregulated genes in PBMCs. Real time qRT-PCR (24 samples each) and in vitro assays were employed to validate our primary findings and hypothesis.
resultsBy RNA-seq analysis of PBMCs, we found that Wnt signaling pathway was upregulated in PTSD when compared to normal controls. Specifically, we found increased expression of WNT10B in the PTSD group when compared to controls. Our findings were confirmed using NCBI's GEO database involving a larger sample size. Additionally, in vitro activation studies revealed that activated but not naïve PBMCs from control individuals expressed more IFNγ in the presence of recombinant WNT10B suggesting that Wnt signaling played a crucial role in exacerbating inflammation. Next, we investigated the mechanism of induction of WNT10B and found that increased expression of WNT10B may result from epigenetic modulation involving downregulation of hsa-miR-7113-5p which targeted WNT10B. Furthermore, we also observed that WNT10B overexpression was linked to higher expression of H3K4me3 histone modification around the promotor of WNT10B. Additionally, knockdown of histone demethylase specific to H3K4me3, using siRNA, led to increased expression of WNT10B providing conclusive evidence that H3K4me3 indeed controlled WNT10B expression.
conclusionsIn summary, our data demonstrate for the first time that Wnt signaling pathway is upregulated in PBMCs of PTSD patients resulting from epigenetic changes involving microRNA dysregulation and histone modifications, which in turn may promote the inflammatory phenotype in such cells.
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