ArticleStem cell research & therapy2021
Upregulation of Apol8 by Epothilone D facilitates the neuronal relay of transplanted NSCs in spinal cord injury.
Article in Stem cell research & therapy, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 18 citations in OpenAlex.
- Harnessing Endogenous Neural Stem Cells: A New Frontier in Spinal Cord Injury Repair.Neurochemical research · 2026Review
- Inhibition of neuronal necroptosis via disruption of RIPK1-RIPK3 Interactions: The role of neural stem cell-derived exosomes in spinal cord injury recovery.Bioactive materials · 2025Article
- Review
- Identification of additional body weight QTLs in the Berlin Fat Mouse BFMI861 lines using time series data.Scientific reports · 2024Article
- The Janus-faced functions of Apolipoproteins L in membrane dynamics.Cellular and molecular life sciences : CMLS · 2024Article
- Spinal cord injury: molecular mechanisms and therapeutic interventions.Signal transduction and targeted therapy · 2023Review
- Developmental stage of transplanted neural progenitor cells influences anatomical and functional outcomes after spinal cord injury in mice.Communications biology · 2023Article
- Advances in Neural Stem Cell Therapy for Spinal Cord Injury: Safety, Efficacy, and Future Perspectives.Neurospine · 2022Article
- Mechanisms of Axon Growth and Regeneration: Moving between Development and Disease.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Microtubule Organization Is Essential for Maintaining Cellular Morphology and Function.Oxidative medicine and cellular longevity · 2022Review
- Catalpol as a Component ofFrontiers in pharmacology · 2022Article
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Authors and funding
13 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMicrotubule-stabilizing agents have been demonstrated to modulate axonal sprouting during neuronal disease. One such agent, Epothilone D, has been used to treat spinal cord injury (SCI) by promoting axonal sprouting at the lesion site after SCI. However, the role of Epothilone D in the differentiation of neural stem cells (NSCs) in SCI repair is unknown. In the present study, we mainly explored the effects and mechanisms of Epothilone D on the neuronal differentiation of NSCs and revealed a potential new SCI treatment.
methodsIn vitro differentiation assays, western blotting, and quantitative real-time polymerase chain reaction were used to detect the effects of Epothilone D on NSC differentiation. Retrograde tracing using a pseudotyped rabies virus was then used to detect neuronal circuit construction. RNA sequencing (RNA-Seq) was valuable for exploring the target gene involved in the neuronal differentiation stimulated by Epothilone D. In addition, lentivirus-induced overexpression and RNA interference technology were applied to demonstrate the function of the target gene. Last, an Apol8-NSC-linear ordered collagen scaffold (LOCS) graft was prepared to treat a mouse model of SCI, and functional and electrophysiological evaluations were performed.
resultsWe first revealed that Epothilone D promoted the neuronal differentiation of cultured NSCs and facilitated neuronal relay formation in the injured site after SCI. Furthermore, the RNA-Seq results demonstrated that Apol8 was upregulated during Epothilone D-induced neuronal relay formation. Lentivirus-mediated Apol8 overexpression in NSCs (Apol8-NSCs) promoted NSC differentiation toward neurons, and an Apol8 interference assay showed that Apol8 had a role in promoting neuronal differentiation under the induction of Epothilone D. Last, Apol8-NSC transplantation with LOCS promoted the neuronal differentiation of transplanted NSCs in the lesion site as well as synapse formation, thus improving the motor function of mice with complete spinal cord transection.
conclusionsEpothilone D can promote the neuronal differentiation of NSCs by upregulating Apol8, which may provide a promising therapeutic target for SCI repair.
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