AI Article Synopsis
- Astrocytes react to brain injuries and can lead to neuron death, but how this happens isn't fully understood; this study investigates the role of a specific microRNA (miRNA-382-5p) found in extracellular vesicles (EVs) as a potential biomarker for traumatic brain injury (TBI).
- The level of EV-miRNA-382-5p rises significantly in TBI patients and model mice, and it disrupts communication between astrocytes and neurons, causing mitochondrial problems by inhibiting a protein called optic atrophy-1 (OPA1).
- Targeting miRNA-382-5p with engineered EVs that deliver an inhibitor can reduce mitochondrial damage and improve neural function, indicating that this micro
Article Abstract
Although astrocytes undergo functional changes in response to brain injury and may be the driving force of subsequent neuronal death, the underlying mechanisms remain incompletely elucidated. Here, we showed that extracellular vesicle (EV)-shuttled miRNA-382-5p may serve as a biomarker for the severity of traumatic brain injury (TBI), as the circulating EV-miRNA-382-5p level was significantly increased in both human patients and TBI model mice. Mechanistically, astrocyte-derived EVs delivered the shuttled miRNA-382-5p to mediate astrocyte-neuron communication, which promoted neuronal mitochondrial dysfunction by inhibiting the expression of optic atrophy-1 (OPA1). Consistent with these findings, genetic ablation of neuronal OPA1 exacerbated mitochondrial damage and neuronal apoptosis in response to TBI. Moreover, engineered RVG-miRNA-382-5p inhibitor-EVs, which can selectively deliver a miRNA-382-5p inhibitor to neurons, significantly attenuated mitochondrial damage and improved neurological function after TBI. Taken together, our data suggest that EV-shuttled miRNA-382-5p may be a critical mediator of astrocyte-induced neurotoxicity under pathological conditions and that targeting miRNA-382-5p-OPA1 signaling has potential for clinical translation in the treatment of traumatic brain injury.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11671591 | PMC |
| http://dx.doi.org/10.1038/s12276-024-01355-3 | DOI Listing |
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