ArticleDevelopmental neuroscience2011
Abnormal microRNA expression in Ts65Dn hippocampus and whole blood: contributions to Down syndrome phenotypes.
Article in Developmental neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.
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Who cites it
21 citing papers in PubMed, 1 synthesis or guideline pooled it, 47 citations in OpenAlex.
- Meta-Analysis of Gene Expression Changes in the Blood of Patients with Mild Cognitive Impairment and Alzheimer's Disease Dementia.International journal of molecular sciences · 2019Pooled it
- The Role of Oxidative Stress in Trisomy 21 Phenotype.Cellular and molecular neurobiology · 2023Review
- Profiling of circulating chromosome 21-encoded microRNAs, miR-155, and let-7c, in down syndrome.Molecular genetics & genomic medicine · 2022Article
- Aging with Down Syndrome-Where Are We Now and Where Are We Going?Journal of clinical medicine · 2021Review
- The Potential Role of miRNAs as Predictive Biomarkers in Neurodevelopmental Disorders.Journal of molecular neuroscience : MN · 2021Review
- Role of mTOR-regulated autophagy in spine pruning defects and memory impairments induced by binge-like ethanol treatment in adolescent mice.Brain pathology (Zurich, Switzerland) · 2021Article
- Comparative analysis of the down syndrome hippocampal non-coding RNA transcriptomes using a mouse model.Genes & genomics · 2020Article
- Inhibition of miR-155 Limits Neuroinflammation and Improves Functional Recovery After Experimental Traumatic Brain Injury in Mice.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2019Article
- hsa-let-7c miRNA Regulates Synaptic and Neuronal Function in Human Neurons.Frontiers in synaptic neuroscience · 2018Article
- Down syndrome and microRNAs.Biomedical reports · 2018Article
- Integrated microRNA and protein expression analysis reveals novel microRNA regulation of targets in fetal down syndrome.Molecular medicine reports · 2016Article
- Genome-wide miR-155 and miR-802 target gene identification in the hippocampus of Ts65Dn Down syndrome mouse model by miRNA sponges.BMC genomics · 2015Article
- miR-155 Is Essential for Inflammation-Induced Hippocampal Neurogenic Dysfunction.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Bias in microRNA functional enrichment analysis.Bioinformatics (Oxford, England) · 2015Article
- Differentially expressed microRNAs in maternal plasma for the noninvasive prenatal diagnosis of Down syndrome (trisomy 21).BioMed research international · 2014Article
- Review
- Weaker control of the electrical properties of cerebellar granule cells by tonically active GABAA receptors in the Ts65Dn mouse model of Down's syndrome.Molecular brain · 2013Article
- Loss of sorting nexin 27 contributes to excitatory synaptic dysfunction by modulating glutamate receptor recycling in Down's syndrome.Nature medicine · 2013Article
- MicroRNAs and intellectual disability (ID) in Down syndrome, X-linked ID, and Fragile X syndrome.Frontiers in cellular neuroscience · 2013Article
- Article
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Down syndrome (DS; trisomy 21) is one of the most common genetic causes of intellectual disability, which is attributed to triplication of genes located on chromosome 21. Elevated levels of several microRNAs (miRNAs) located on chromosome 21 have been reported in human DS heart and brain tissues. The Ts65Dn mouse model is the most investigated DS model with a triplicated segment of mouse chromosome 16 harboring genes orthologous to those on human chromosome 21. Using ABI TaqMan miRNA arrays, we found a set of miRNAs that were significantly up- or downregulated in the Ts65Dn hippocampus compared to euploid controls. Furthermore, miR-155 and miR-802 showed significant overexpression in the Ts65Dn hippocampus, thereby confirming results of previous studies. Interestingly, miR-155 and miR-802 were also overexpressed in the Ts65Dn whole blood but not in lung tissue. We also found overexpression of the miR-155 precursors, pri- and pre-miR-155 derived from the miR-155 host gene, known as B cell integration cluster, suggesting enhanced biogenesis of miR-155. Bioinformatic analysis revealed that neurodevelopment, differentiation of neuroglia, apoptosis, cell cycle, and signaling pathways including ERK/MAPK, protein kinase C, phosphatidylinositol 3-kinase, m-TOR and calcium signaling are likely targets of these miRNAs. We selected some of these potential gene targets and found downregulation of mRNA encoding Ship1, Mecp2 and Ezh2 in Ts65Dn hippocampus. Interestingly, the miR-155 target gene Ship1 (inositol phosphatase) was also downregulated in Ts65Dn whole blood but not in lung tissue. Our findings provide insights into miRNA-mediated gene regulation in Ts65Dn mice and their potential contribution to impaired hippocampal synaptic plasticity and neurogenesis, as well as hemopoietic abnormalities observed in DS.
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Registered trials
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