ArticleScientific reports2017
Enhanced derivation of human pluripotent stem cell-derived cortical glutamatergic neurons by a small molecule.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 1 of them a synthesis that pooled it.
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45 citing papers in PubMed, 1 synthesis or guideline pooled it.
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- Intersecting impact of CAG repeat and huntingtin knockout in stem cell-derived cortical neurons.Neurobiology of disease · 2025Article
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- Elevated p16Ink4a Expression Enhances Tau Phosphorylation in Neurons Differentiated From Human-Induced Pluripotent Stem Cells.Aging cell · 2025Article
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- Harnessing the potential of human induced pluripotent stem cells, functional assays and machine learning for neurodevelopmental disorders.Frontiers in neuroscience · 2024Review
- Directional induction of neural stem cells, a new therapy for neurodegenerative diseases and ischemic stroke.Cell death discovery · 2023Review
- Cerebral organoids transplantation repairs infarcted cortex and restores impaired function after stroke.NPJ Regenerative medicine · 2023Article
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9 authors.
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Abstract
Human pluripotent stem cells (hPSCs) play important role in studying the function of human glutamatergic neurons and related disease pathogenesis. However, the current hPSC-derived cortical system produced a significant number of inhibitory GABAergic neurons that reduced the purity of excitatory neurons. In this study, we established a robust hPSC-derived cortical neurogenesis system by applying the SHH inhibitor cyclopamine. Cyclopamine specified the dorsal cortical fate in a dose-dependent manner and enhanced the generation of cortical glutamatergic neurons, expressing PAX6, TBR1, TBR2, CTIP2, SATB2, and vesicular glutamate transporters (vGLUT). In contrast, the ventral patterning was inhibited and the GABAergic neurons were significantly reduced to 12% with the treatment of cyclopamine. In addition, we applied our current method to generate trisomy 21 iPSC-derived glutamatergic neurons that showed a robust reduction of vesicular glutamate transporters in the glutamatergic neurons with trisomy 21, revealing the developmental deficits in cortical glutamatergic neurons. Our method enriched the generation of cortical glutamatergic neurons which may facilitate the study of human neurological diseases and cell therapy.
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