ArticleJournal of Korean Neurosurgical Society2026
Treatment with Neuronal-Induced Human Mesenchymal Stem Cells Improves Functional Recovery of Acute Spinal Cord Injury through Attenuating Astrogliosis and Neurotoxic Astrocyte Activation.
Article in Journal of Korean Neurosurgical Society, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
- Editors' Pick in September 2026.Journal of Korean Neurosurgical Society · 2026Article
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6 authors.
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Abstract
objectiveMost of the preclinical studies have been focusing on inhibition of astrogliosis which is known as a major mechanism that inhibits recovery from spinal cord injury (SCI). Although mesenchymal stem cells (MSCs) have been widely studied as therapeutic candidates for SCI treatment, the role of MSCs on astrogliosis remains unclear. Furthermore, recent studies revealed that astrogliosis also has a protective role in SCI. The purpose of this study was to determine whether neural-induced human adipose tissue-derived MSCs (NIhADSCs) promote SCI repair through astrogliosis modulation.
methodsNI-hADSCs were transplanted into the perilesional spinal cord in an acute severe SCI rat model. Functional recovery was evaluated serially on postoperative day 1 and weekly thereafter for 6 weeks using the Basso-Beattie-Bresnahan (BBB) locomotor rating scale. Western blot analysis was performed to assess protein levels of gliosis markers and neuroinflammatory pathways at 6 weeks post-injury. Histopathological examination was conducted at 6 weeks post-injury to evaluate astrogliosis and astrocyte phenotypic changes.
resultsNI-hADSC transplantation significantly improved functional recovery compared with the SCI group, as demonstrated by a greater cumulative BBB locomotor score over 6 weeks (area under the curve : 23.65 vs. 13.58; p=0.026). At 6 weeks post-injury, the levels of glial fibrillary acidic protein (0.52±0.11 vs. 1.00±0.12; p=0.012), vimentin (0.54±0.01 vs. 1.00±0.08; p=0.006), and complement component 3 (C3; 0.38±0.05 vs. 1.00±0.07; p<0.001) in the NI-hADSC-treated group were markedly decreased, whereas the levels of signal transducer and activator of transcription 3 (STAT3)/phosphorylated STAT3 proteins were markedly increased (1.51±0.18 vs. 1.00±0.14; p<0.05). The levels of S100 calcium-binding protein A10 and nuclear factor kappa B (NFκB)/phosphorylated NFκB expression showed no significant differences between groups. Immunohistochemistry confirmed reduced astrogliosis and fewer C3-expressing astrocytes in the NI-hADSC-treated group, predominantly in the dorsal perilesional spinal cord. Substantially increased B-cell lymphoma-2 (Bcl-2) expression (14.30±2.13 vs. 5.86±0.66; p<0.01) and decreased Bcl-2-associated X protein expression (58.64%±2.82% vs. 69.46%±1.81%; p<0.01) indicated that NI-hADSC treatment reduced neuronal apoptosis.
conclusionNI-hADSC transplantation improved functional recovery in SCI by modulating astrogliosis. The modulation of astrogliosis was likely to be achieved through selective suppression of detrimental A1 astrocytes, potentially via STAT3 signaling. However, the protective effect of NI-hADSCs on astrogliosis diminished during the subacute SCI period and was spatially restricted to the perilesional area.
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