1. Academic Validation
  2. Role of neuroglia cell-derived microvesicles in cobalt chloride-induced mitochondrial autophagy in neurons

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

  • Toxicology. 2025 Jun 7:517:154214. doi: 10.1016/j.tox.2025.154214.
Husheng Li 1 Fuli Zheng 2 Wenya Shao 2 Guangxia Yu 2 Hong Hu 2 Zhenkun Guo 1 Siying Wu 3 Ying Tang 4 Huangyuan Li 5
Affiliations

Affiliations

  • 1 Department of Preventive Medicine, School of Public Health, Fujian Medical University, Fuzhou 350122, China.
  • 2 Department of Preventive Medicine, School of Public Health, Fujian Medical University, Fuzhou 350122, China; The Key Laboratory of Environment and Health, School of Public Health, Fujian Medical University, Fuzhou 350122, China.
  • 3 The Key Laboratory of Environment and Health, School of Public Health, Fujian Medical University, Fuzhou 350122, China; Department of Epidemiology and Health Statistics, School of Public Health, Fujian Medical University, Fuzhou 350122, China. Electronic address: sywu@fjmu.edu.cn.
  • 4 Fujian Center for Prevention and Control of Occupational Diseases and Chemical Poisoning, Fuzhou 350125, China. Electronic address: 528392655@qq.com.
  • 5 Department of Preventive Medicine, School of Public Health, Fujian Medical University, Fuzhou 350122, China; The Key Laboratory of Environment and Health, School of Public Health, Fujian Medical University, Fuzhou 350122, China. Electronic address: fmulhy@163.com.
Abstract

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.

Keywords

Cellular microvesicles; Cobalt chloride; Mitochondrial autophagy; Neuronal damage.

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