Role of neuroglia cell-derived microvesicles in cobalt chloride-induced mitochondrial autophagy in neurons.

The extensive use of cobalt resources has significantly increased the risk of cobalt contamination globally, with cobalt chloride posing a serious environmental and health concern. Although previous studies have shown that extracellular vesicles play a key role in intercellular communication, the mechanisms by which extracellular vesicles derived from neuroglia cells affect neuronal cells remain poorly understood. This study aimed to investigate whether microvesicles produced by neuroglia cells could mitigate cobalt chloride-induced neuronal damage and to explore the underlying mechanisms. Our results revealed that cobalt chloride induces cytotoxicity in HT22 and MN9D neuronal cells. A 24-hour cobalt chloride treatment triggered mitochondrial autophagy in both cell types and disrupted their mitochondrial dynamics. Further analysis showed that microvesicles secreted by GL261 neuroglia cells were taken up by both types of neuronal cells. Notably, the uptake of GL261-derived microvesicles by MN9D cells inhibited autophagy and restored mitochondrial membrane potential and reactive oxygen species levels. In conclusion, our findings highlight the critical role of neuroglia cell-derived microvesicles in cobalt chloride-induced neuronal toxicity and offer potential new targets and strategies for the prevention and treatment of cobalt chloride toxicity.