This study finds that olfactory mucosa MSC-derived exosomes improve outcomes after intracranial hemorrhage, suggesting a role for miR-30b-5p in neuroprotection.
Exosomes derived from olfactory mucosa mesenchymal stem cells (OM‐MSCs‐EXOs) offer a novel therapeutic strategy for various diseases due to their role in regulating intercellular signaling. However, the potential of OM‐MSCs‐EXOs to improve intracranial hemorrhage (ICH) and its underlying mechanisms is unclear. In this study, we found that OM‐MSCs‐EXOs can perfect neurofunctional recovery after ICH. The level of miR‐30b‐5p declined in thrombin‐triggered OM‐MSCs. Suppression of miR‐30b‐5p in OM‐MSCs‐EXOs inhibited mitophagy and promoted reactive oxygen species (ROS) and inflammasome‐related protein levels. Moreover, downregulation of miR‐30b‐5p in OM‐MSCs‐EXOs inhibited HT22 cell viability and promoted apoptosis and inflammation. Mechanistically, miR‐30b‐5p targeted SENP5 and decreased the level of SENP5. SENP5 silencing upregulated SUMO2/3‐conjugated METTL3 and downregulated METTL3 levels. METTL3 silencing inhibited LPA1 levels by inhibiting m6A modifications. Further, SUMOylated METTL3 was decreased and the m6A level of LPA1 was enhanced in thrombin‐triggered BV2 cells, which was abolished by OM‐MSCs‐EXOs, and this phenomenon was reversed by miR‐30b‐5p silenced‐OM‐MSCs‐EXOs. This work confirmed the potential of OM‐MSCs‐EXOs mediated delivery of miR‐30b‐5p in relieving ICH via the SENP5/METTL3/LPA1 axis.
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Gao et al. (2025) studied this question.
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