ArticleAnimal models and experimental medicine2025
Transplanting neural stem cells overexpressing miRNA-21 can promote neural recovery after cerebral hemorrhage through the SOX2/LIN28-let-7 signaling pathway.
Article in Animal models and experimental medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Cell therapy comparison of dental pulp stem cells, hepatocytes, and their exosomes for liver fibrosis treatment in rats.Animal models and experimental medicine · 2026Article
- The role of stem cells and their engineering strategies in the repair of nerve damage in intracerebral hemorrhage.Cell & bioscience · 2026Review
- Emerging Therapeutic Strategies in Intracerebral Hemorrhage: Enhancing Neurogenesis and Functional Recovery.MedComm · 2025Review
- Transplanting neural stem cells overexpressing miRNA-21 can promote neural recovery after cerebral hemorrhage through the SOX2/LIN28-let-7 signaling pathway.Animal models and experimental medicine · 2025Article
- Advances in Expression Regulation, Molecular Targeting Mechanisms, and Therapeutic Applications of the Let-7 MicroRNA Family in Gastric Cancer.Oncology research · 2025Review
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Authors and funding
8 authors.
Funding
Abstract
backgroundIntracerebral hemorrhage (ICH) remains a devastating neurological disorder with limited therapeutic options. Neural stem cell (NSC)-based therapies have emerged as a potential regenerative approach, yet the molecular mechanisms regulating NSC behavior require further elucidation. The role of miR-21 in NSC differentiation and proliferation during ICH recovery remains unexplored.
methodsIn vitro NSC cultures were analyzed for miR-21 expression dynamics during differentiation via qPCR. Lentiviral overexpression and knockdown of miR-21 were employed to assess its functional impact. The SOX2/LIN28-let-7 pathway was investigated using Western blot, luciferase reporter assays, and immunofluorescence. In vivo, miR-21-overexpressing NSCs were transplanted into a murine ICH model, with neurogenesis evaluated by immunostaining and neurological recovery assessed through behavioral tests (mNSS, rotarod).
resultsmiR-21 expression significantly increased during NSC differentiation, correlating with reduced SOX2 levels. Mechanistically, miR-21 directly targeted SOX2, disrupting the SOX2/LIN28-let-7 axis to promote NSC proliferation and lineage commitment. In ICH mice, transplantation of miR-21-overexpressing NSCs enhanced neurogenesis and improved motor coordination and neurological deficits at 28 days post-transplantation.
conclusionsOur findings identify miR-21 as a critical regulator of NSC plasticity through SOX2/LIN28-let-7 signaling, highlighting its therapeutic potential for enhancing neuroregeneration and functional recovery in ICH. Targeting miR-21 may represent a novel strategy to optimize NSC-based therapies for hemorrhagic stroke.
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