ArticleBrain and behavior2020
Hypoxic preconditioning enhances the differentiation of bone marrow stromal cells into mature oligodendrocytes via the mTOR/HIF-1α/VEGF pathway in traumatic brain injury.
Article in Brain and behavior, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 3 of them syntheses that pooled it.
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Who cites it
13 citing papers in PubMed, 3 syntheses or guidelines pooled it, 11 citations in OpenAlex.
- Adipose-Derived Stem Cells in Traumatic Brain Injury: A Systematic Review of Preclinical Studies.Tissue engineering and regenerative medicine · 2026Pooled it
- Pooled it
- Evolution of mesenchymal stem cell therapies for traumatic brain injury: A decade of advances, mechanisms, and translational prospects.Cell transplantationPooled it
- Quieting the Storm: Hypoxia as a Strategy to Boost UC-MSC Therapies for Hypoxic-Ischemic Brain Lesions in Neonatal Rats.Stem cell reviews and reports · 2026Article
- Review
- The application of mesenchymal stem cells in the treatment of traumatic brain injury: Mechanisms, results, and problems.Histology and histopathology · 2024Review
- Effects of bone marrow mesenchymal stromal cells-derived therapies for experimental traumatic brain injury： A meta-analysis.Heliyon · 2024Article
- [Research progress on mechanism of traumatic brain injury promoting fracture healing].Zhongguo xiu fu chong jian wai ke za zhi = Zhongguo xiufu chongjian waike zazhi = Chinese journal of reparative and reconstructive surgery · 2024Article
- Article
- Identification of novel key markers that are induced during traumatic brain injury in mice.PeerJ · 2023Article
- Systematic review and meta-analysis of preclinical studies testing mesenchymal stromal cells for traumatic brain injury.NPJ Regenerative medicine · 2021Article
- Maternal Vit D supplementation in AMA mice and the role of Vit D/VDR signaling in the offspring's cognition.American journal of translational research · 2021Article
- Hypoxic preconditioning enhances the differentiation of bone marrow stromal cells into mature oligodendrocytes via the mTOR/HIF-1α/VEGF pathway in traumatic brain injury.Brain and behavior · 2020Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
objectiveTraumatic brain injury (TBI) results not only in gray matter damage, but also in severe white matter injury (WMI). Previous findings support hypoxic preconditioning (HP) could augment the efficacy of bone marrow stromal cell (BMSC) transplantation in a TBI mouse model. However, whether HP-treated BMSCs (H-BMSCs) could overcome remyelination failure after WMI is unclear, and the molecular mechanisms remain to be explored. Here, we focused on the therapeutic benefits of H-BMSC transplantation for treating WMI, as well as its underlying mechanisms.
methodsIn vitro, BMSCs were incubated at passage 4 in the hypoxic preconditioning (1.0% oxygen) for 8 hr. In vivo, a TBI mouse model was established, and DMEM cell culture medium (control), normal cultured BMSCs (N-BMSCs), or H-BMSCs were transplanted to mice 24 hr afterward. Neurobehavioral function, histopathological changes, and oligodendrogenesis were assessed for up to 35 days post-TBI.
resultsCompared with the control group, improvement of cognitive functions and smaller lesion volumes was observed in the two BMSC-transplanted groups, especially the H-BMSC group. H-BMSC transplantation resulted in a greater number of neural/glial antigen 2 (NG2)-positive and adenomatous polyposis coli (APC)-positive cells than N-BMSC transplantation in both the corpus callosum and the striatum. In addition, we observed that the expression levels of hypoxia-inducible factor-1a (HIF-1α), phosphorylated mechanistic target of rapamycin (p-mTOR), and vascular endothelial growth factor (VEGF) were all increased in H-BMSC-transplanted mice. Furthermore, the mTOR pathway inhibitor rapamycin attenuated the impact of HP both in vivo and in vitro.
conclusionThe results provided mechanistic evidences suggesting that HP-treated BMSCs promoted remyelination partly by modulating the pro-survival mTOR/HIF-1α/VEGF signaling pathway.
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