Over-expression microRNA-218 induces differentiation of neural stem cells into functional motor neuron-like cells with differential expression of PI3K/Akt/mTOR, PTEN and GSK3ß signaling proteins.
Khalil W., Tiraihi T., Shojaei A., Hassoun HK.
Animal Study, published in Life Sci (2025) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Animal Study
- Journal
- Life Sci (2025)
- Country
- Netherlands
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 41083122
- DOI
- 10.1016/j.lfs.2025.124015
Abstract (original English)
Aims Functional motor neurons derived from stem cells can be used for in vitro modeling or future preclinical applications of neuronal disorders. When the stem cells are regulated by miRNAs, they target many signaling pathways, including PI3K/Akt/mTOR cascade. The level of protein expression of PI3K/Akt/mTOR, PTEN and GSK3ß pathways are evaluated in the motor neuron-like cells (MNLC). Materials and methods The neural stem cells (NSC) were transdifferentiated from adipose-derived mesenchymal stem cells (ADMSC) and transduced with miRNA-218 lentiviral vector, generating MNLC. ADMSC, NSC, and MNLC were characterized and the functionality of the MNLC was evaluated by qRT-PCR and patch clamp recording. The ADMSC were immunoreactive to CD49d, CD73, CD90, and CD44. Key findings The results of RT-PCR show the expression of nestin, Neurod1, GAP43, neurofilament 68 and neurogenin genes in NSC. The MNLC showed a significant increase in the expression of neurofilament 200, synaptophysin, motor neuron markers ISLET1, Olig2, and HB9, as well as the functionality genes. The MNLC co-cultured with myofibers showed myofibers innervation and produced action potential detected by patch clamp recording. The expression level of PI3K/Akt/mTOR pathway members decreased, while its antagonists PTEN and GSK3ß pathways increased. Significance These findings show the induction of NSC into MNLC by microRNA
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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