ArticleInternational journal of stem cells2023
Transcriptional Signature of Valproic Acid-Induced Neural Tube Defects in Human Spinal Cord Organoids.
Article in International journal of stem cells, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 15 citations in OpenAlex.
- hiPSC-derived Organoids and Organ-on-chip Systems: New Frontiers in Neural Tube Defect Research.Stem cell reviews and reports · 2026Review
- Multiomics analysis identifies VPA-induced changes in neural progenitor cells, ventricular-like regions, and cellular microenvironment in dorsal forebrain organoids.Molecular psychiatry · 2026Article
- Enhanced U-Net-Based Deep Learning Model for Automated Segmentation of Organoid Images.Bioengineering (Basel, Switzerland) · 2025Article
- Towards a quality control framework for cerebral cortical organoids.Scientific reports · 2025Article
- Human organoids potentially boost research into environmental factors of neural tube defects.Reproductive toxicology (Elmsford, N.Y.) · 2025Review
- Generation of Neural Organoids and Their Application in Disease Modeling and Regenerative Medicine.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- Valproic acid-induced teratogenicity is driven by senescence and prevented by Rapamycin in human spinal cord and animal models.Molecular psychiatry · 2025Article
- Toxicity assessment using neural organoids: innovative approaches and challenges.Toxicological research · 2025Review
- The Differential Developmental Neurotoxicity of Valproic Acid on Anterior and Posterior Neural Induction of Human Pluripotent Stem Cells.International journal of stem cells · 2025Article
- Polarization of organoids by bioengineered symmetry breaking.IBRO neuroscience reports · 2024Article
- A Roadmap for Selecting and Utilizing Optimal Features in scRNA Sequencing Data Analysis for Stem Cell Research: A Comprehensive Review.International journal of stem cells · 2024Review
- ASCL1-mediated direct reprogramming: converting ventral midbrain astrocytes into dopaminergic neurons for Parkinson's disease therapy.BMB reports · 2024Article
- Establishment and Validation of a Model for Fetal Neural Ischemia Using Necrotic Core-Free Human Spinal Cord Organoids.Stem cells translational medicine · 2024Article
- Progress in spinal cord organoid research: advancing understanding of neural development, disease modelling, and regenerative medicine.Biomaterials translational · 2024Review
Corrections and comments
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4 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
In vertebrates, the entire central nervous system is derived from the neural tube, which is formed through a conserved early developmental morphogenetic process called neurulation. Although the perturbations in neurulation caused by genetic or environmental factors lead to neural tube defects (NTDs), the most common congenital malformation and the precise molecular pathological cascades mediating NTDs are not well understood. Recently, we have developed human spinal cord organoids (hSCOs) that recapitulate some aspects of human neurulation and observed that valproic acid (VPA) could cause neurulation defects in an organoid model. In this study, we identified and verified the significant changes in cell-cell junctional genes/proteins in VPA-treated organoids using transcriptomic and immunostaining analysis. Furthermore, VPA-treated mouse embryos exhibited impaired gene expression and NTD phenotypes, similar to those observed in the hSCO model. Collectively, our data demonstrate that hSCOs provide a valuable biological resource for dissecting the molecular pathways underlying the currently unknown human neurulation process using destructive biological analysis tools.
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Registered trials
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.