Published online Feb 26, 2025. doi: 10.4252/wjsc.v17.i2.101395
Revised: December 27, 2024
Accepted: February 11, 2025
Published online: February 26, 2025
Processing time: 87 Days and 22.6 Hours
Epilepsy is a prevalent chronic neurological disorder affecting 50 million individuals globally, with temporal lobe epilepsy (TLE) being the most common form. Despite advances in antiepileptic drug development, over 30% of patients suffer from drug-resistant epilepsy, which can lead to severe cognitive impair
To explore the role of bone marrow mesenchymal stem cell (BMSC)-derived exosomal miR-203 in the regulation of neuroinflammation in a mouse model of epilepsy, providing a theoretical basis for the development of targeted microRNA delivery therapies for drug-resistant epilepsy.
Adult male C57BL/6 mice were divided into a control group and a TLE model of 30 mice each, and the TLE model group was established by injecting kainic acid. BMSCs were isolated from the mice, and exosomes were purified using ultracentrifugation. Exosomal miR-203 was identified and characterized using high-throughput sequencing and quantitative reverse-transcription polymerase chain reaction. The uptake of exosomes by hippocampal neurons and the subsequent effects on neuroinflammatory markers were assessed using in vitro cell culture models.
Exosomal miR-203 exhibited a significant upregulation in BMSCs derived from epileptic mice. In vitro investigations demonstrated the efficient internalization of these exosomes by hippocampal neurons, resulting in downregulation of sup
Our study identifies exosomal miR-203 as a key regulator of neuroinflammation in a mouse model of epilepsy. The findings suggest that targeting miR-203 may offer a novel therapeutic strategy for epilepsy by modulating the suppression of cytokine signaling 3/nuclear factor kappaB pathway, thus providing a potential avenue for the development of cell-free therapeutics.
Core Tip: This study highlights the role of bone marrow mesenchymal stem cell-derived exosomal miR-203 in regulating neuroinflammation in a mouse model of temporal lobe epilepsy. These findings suggest that miR-203 modulates the suppressor of cytokine signaling 3/nuclear factor kappaB pathway, leading to increased neuroinflammation. This pathway activation promotes the secretion of proinflammatory cytokines, contributing to the pathology of epilepsy. Targeting miR-203 may offer a novel therapeutic approach for drug-resistant epilepsy by reducing neuroinflammation and improving patient outcomes, offering potential for future cell-free therapeutic strategies.