ArticleTranslational psychiatry2016
Analysis of induced pluripotent stem cells carrying 22q11.2 deletion.
Article in Translational psychiatry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers, 1 of them a synthesis that pooled it.
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Who cites it
68 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Mental health dished up-the use of iPSC models in neuropsychiatric research.Journal of neural transmission (Vienna, Austria : 1996) · 2020Pooled it
- Gene dosage effects of 22q11.2 copy number variants on in-vivo measures of white matter axonal density and dispersion.Molecular psychiatry · 2026Article
- Exploring the roots of schizophrenia: Current research and future directions (Review).Experimental and therapeutic medicine · 2026Review
- How copy number variations shape brain developmental disorders: Unraveling the synaptic puzzle.Psychiatry and clinical neurosciences · 2026Review
- Extracellular matrix dysfunction and synaptic alterations in schizophrenia.Molecular psychiatry · 2026Article
- Aberrant pace of cortical neuron development in brain organoids from patients with 22q11.2 deletion syndrome-associated schizophrenia.Nature communications · 2025Article
- ESC models of autism with copy-number variations reveal cell-type-specific translational vulnerability.Cell genomics · 2025Article
- Fine Regulation of MicroRNAs in Gene Regulatory Networks and Pathophysiology.International journal of molecular sciences · 2025Review
- Modeling common and rare genetic risk factors of neuropsychiatric disorders in human induced pluripotent stem cells.Schizophrenia research · 2024Review
- Probing the molecular and cellular pathological mechanisms of schizophrenia using human induced pluripotent stem cell models.Schizophrenia research · 2024Review
- Patient iPSC-derived neural progenitor cells display aberrant cell cycle control, p53, and DNA damage response protein expression in schizophrenia.BMC psychiatry · 2024Article
- Next-generation sequencing profiling of miRNAs in individuals with 22q11.2 deletion syndrome revealed altered expression of miR-185-5p.Human genomics · 2024Article
- Analysis of human neuronal cells carrying ASTN2 deletion associated with psychiatric disorders.Translational psychiatry · 2024Article
- Comparing stem cells, transdifferentiation and brain organoids as tools for psychiatric research.Translational psychiatry · 2024Review
- Copy Number Variations in Neuropsychiatric Disorders.International journal of molecular sciences · 2023Review
- Mitochondrial proteins encoded by the 22q11.2 neurodevelopmental locus regulate neural stem and progenitor cell proliferation.Molecular psychiatry · 2023Article
- Novel Compounds in the Treatment of Schizophrenia-A Selective Review.Brain sciences · 2023Review
- Unlocking Neural Function with 3D In Vitro Models: A Technical Review of Self-Assembled, Guided, and Bioprinted Brain Organoids and Their Applications in the Study of Neurodevelopmental and Neurodegenerative Disorders.International journal of molecular sciences · 2023Review
- Shedding light on latent pathogenesis and pathophysiology of mental disorders: The potential of iPS cell technology.Psychiatry and clinical neurosciences · 2023Review
- A CRISPR-engineered isogenic model of the 22q11.2 A-B syndromic deletion.Scientific reports · 2023Article
8 more citing papers are in PubMed but not listed here.
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Authors and funding
16 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Given the complexity and heterogeneity of the genomic architecture underlying schizophrenia, molecular analyses of these patients with defined and large effect-size genomic defects could provide valuable clues. We established human-induced pluripotent stem cells from two schizophrenia patients with the 22q11.2 deletion (two cell lines from each subject, total of four cell lines) and three controls (total of four cell lines). Neurosphere size, neural differentiation efficiency, neurite outgrowth, cellular migration and the neurogenic-to-gliogenic competence ratio were significantly reduced in patient-derived cells. As an underlying mechanism, we focused on the role of DGCR8, a key gene for microRNA (miRNA) processing and mapped in the deleted region. In mice, Dgcr8 hetero-knockout is known to show a similar phenotype of reduced neurosphere size (Ouchi et al., 2013). The miRNA profiling detected reduced expression levels of miRNAs belonging to miR-17/92 cluster and miR-106a/b in the patient-derived neurospheres. Those miRNAs are reported to target p38α, and conformingly the levels of p38α were upregulated in the patient-derived cells. p38α is known to drive gliogenic differentiation. The inhibition of p38 activity by SB203580 in patient-derived neurospheres partially restored neurogenic competence. Furthermore, we detected elevated expression of GFAP, a gliogenic (astrocyte) marker, in postmortem brains from schizophrenia patients without the 22q11.2 deletion, whereas inflammation markers (IL1B and IL6) remained unchanged. In contrast, a neuronal marker, MAP2 expressions were decreased in schizophrenia brains. These results suggest that a dysregulated balance of neurogenic-to-gliogenic competence may underlie neurodevelopmental disorders such as schizophrenia.
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