ArticleCell death & disease2017
Epothilone B impairs functional recovery after spinal cord injury by increasing secretion of macrophage colony-stimulating factor.
Article in Cell death & disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 15 citations in OpenAlex.
- High-throughput chemical screen identifies epothilone B in modulating inflammatory bowel disease by triggering neutrophil apoptosis.Genes & diseases · 2027Article
- Identification of a NUAK1/2 Inhibitor as a Macrophage-Polarizing Compound by a Machine Learning-Based Phenotypic Cell Painting Screen.International journal of molecular sciences · 2026Article
- Microtubules in Spinal Cord Injury: From Cytoskeletal Dysregulation to Therapeutic Regeneration.Journal of neurochemistry · 2026Review
- Nanoparticle and epothilone D combinatorial intervention improves motor performance and regeneration in chronic cervical spinal cord injury.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Article
- Fidgetin-like 2 knockdown increases acute neuroinflammation and improves recovery in a rat model of spinal cord injury.Journal of neuroinflammation · 2025Article
- Recent progress and challenges in the treatment of spinal cord injury.Protein & cell · 2023Review
- Effects of Epothilone Administration on Locomotion Recovery after Spinal Cord Injury: A Systematic Review of Animal Studies.Asian spine journal · 2023Article
- Review
- Microtubule-modulating Agents in the Fight Against Neurodegeneration: Will it ever Work?Current neuropharmacology · 2022Review
- Granulocyte-macrophage colony-stimulating factor mRNA and Neuroprotective Immunity in Parkinson's disease.Biomaterials · 2021Article
- Efficacy of epothilones in central nervous system trauma treatment: what has age got to do with it?Neural regeneration research · 2021Article
- The translational landscape in spinal cord injury: focus on neuroplasticity and regeneration.Nature reviews. Neurology · 2019Review
- Knockdown of Fidgetin Improves Regeneration of Injured Axons by a Microtubule-Based Mechanism.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- Epothilone B Benefits Nigral Dopaminergic Neurons by Attenuating Microglia Activation in the 6-Hydroxydopamine Lesion Mouse Model of Parkinson's Disease.Frontiers in cellular neuroscience · 2018Article
- Polycaprolactone electrospun fiber scaffold loaded with iPSCs-NSCs and ASCs as a novel tissue engineering scaffold for the treatment of spinal cord injury.International journal of nanomedicine · 2018Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The microtubule-stabilizing drug epothilone B (epoB) has shown potential value in the treatment of spinal cord injury (SCI) through diverse mechanisms. However, it remains elusive why a limited overall effect was observed. We aim to investigate the limiting factors underlying functional recovery promoted by epoB. The same SCI model treated by epoB was established as discussed previously. We used a cerebrospinal fluid (CSF) sample to assess the changes in cytokines in milieu of the SCI lesion site after epoB treatment. We then analyzed the source of cytokines, the state of microglia/macrophages/monocytes (M/Ms), and the recruitment of neutrophil in the lesion site by using the results of antibody array. Following these findings, we further evaluated the motor functional recovery caused by the reshaped microenvironment. Systemic administration of epoB significantly increased levels of several cytokines in the CSF of the rat SCI model; macrophage colony-stimulating factor (M-CSF) secreted by intact central nervous system (CNS) cells was one of the cytokines with increased levels. Along with epoB and other cytokines, M-CSF reshapes the SCI milieu by activating the microglias, killing bone marrow-derived macrophages, polarizing the M/M to M1 phenotype, and activating downstream cytokines to exacerbate the SCI injury, but it also increases the expression of neurotrophic factors. Anti-inflammatory therapy using a neutralizing antibody mix shows encouraging results. Using in vivo experiments, our findings indicate that epoB inhibits the SCI functional recovery in many ways by reshaping the milieu, which counteracts the therapeutic efficacy that led to the limited overall effectiveness.
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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.