Publications by authors named "Chen-Zi Gong"

Human pluripotent stem cell (hPSC)-derived neurons have shown promise in treating spinal cord injury (SCI). We previously showed that hPSC-derived dorsal spinal γ-aminobutyric acid (GABA) neurons can alleviate spasticity and promote locomotion in rats with SCI, but their long-term safety remains elusive. Here, we characterized the long-term fate and safety of human dorsal spinal GABA neural progenitor cells (NPCs) in naive rats over one year.

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Article Synopsis
  • Spinal interneurons (INs) play a crucial role in regulating nerve signals and movement patterns in the spinal cord, making them important for potential therapies related to spinal injuries and diseases.
  • The study develops a reproducible protocol to create inhibitory GABAergic INs from human pluripotent stem cells through a series of steps, including inducing neuroepithelia and differentiating them into mature neurons.
  • The protocol utilizes small molecules, specifically retinoic acid and cyclopamine, to effectively guide the development of spinal dI4 progenitors, which can enhance research into spinal IN development and create new treatments for spinal cord issues.
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Article Synopsis
  • Spinal cord injury (SCI) commonly leads to spasticity, and there is currently no effective treatment for this condition.
  • Researchers have developed a method to transform human pluripotent stem cells into spinal GABA neurons, which can be used in treatment.
  • When transplanted into rats with spinal cord injuries, these GABA neurons improved movement and reduced spasticity, especially when activated by a specific drug.
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Background: Human embryonic stem cells (hESC) have been an invaluable research tool to study motor neuron development and disorders. However, transcriptional regulation of multiple temporal stages from ESCs to spinal motor neurons (MNs) has not yet been fully elucidated. Thus, the goals of this study were to profile the time-course expression patterns of lncRNAs during MN differentiation of ESCs and to clarify the potential mechanisms of the lncRNAs that are related to MN differentiation.

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Glutamatergic dysregulation has served as one common pathophysiology of major depressive disorder (MDD) and a promising target for treatment intervention. Previous studies implicate neurotransmission via metabotropic glutamate receptors (mGluRs) and Homer1 in stress-induced anhedonia, but the mechanisms have not been well elucidated. In the present study, we used two different animal models of depression, chronic social defeat stress (CSDS) and chronic restraint stress (CRS), to investigate the expression of Homer1 isoforms and functional interaction with mGluRs.

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