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The role of BTG2/PI3K/AKT pathway-mediated microglial activation in T-2 toxin-induced neurotoxicity
Xiukuan Li1, Jinyun Long1, Chunyan Yao2
1School of Public Health, the key Laboratory of Environmental Pollution Monitoring and Disease Control, Ministry of Education, Guizhou Medical University, Guiyang 561113, China; Department of Epidemiology, College of Preventive Medicine, State Key Laboratory of Trauma and Chemical Poisoning, Army Medical University (Third Military Medical University), Chongqing 400038, China.
Abstract:
T-2 toxin is one of the mycotoxins widely distributed in human food and animal feed. Our recent work has shown that microglial activation may contribute to T-2 toxin-induced neurotoxicity. However, the molecular mechanisms involved need to be further clarified. To address this, we employed high-throughput transcriptome sequencing and found altered B cell translocation gene 2 (BTG2) expression levels in microglia following T-2 toxin treatment. It has been shown that altered BTG2 expression is involved in a range of neurological pathologies, but whether it's involved in the regulation of microglial activation is unclear. The aim of this study was to investigate the role of BTG2 in T-2 toxin-induced microglial activation. The results of animal experiments showed that T-2 toxin caused neurobehavioral disorders and promoted the expression of microglial BTG2 and pro-inflammatory activation of microglia in hippocampus and cortical, while microglial inhibitor minocycline inhibited these changes. The results of in vitro experiments showed that T-2 toxin enhanced BTG2 expression and pro-inflammatory microglial activation, and inhibited BTG2 expression weakened T-2 toxin-induced microglial activation. Moreover, T-2 toxin activated PI3K/AKT and its downstream NF-κB signaling pathway, which could be reversed after knock-down of BTG2 expression. Meanwhile, the PI3K inhibitor LY294002 also blocked this process. Therefore, BTG2 may be involved in T-2 toxin's ability to cause microglial activation through PI3K/AKT/NF-κB pathway.
Insights
T-2 toxin exposure activates microglia and alters B cell translocation gene 2 (BTG2) expression, contributing to neurotoxicity. BTG2 plays a key role in T-2 toxin-induced microglial activation via the PI3K/AKT/NF-κB pathway.
Area of Science:
- Neuroscience
- Toxicology
- Molecular Biology
Background:
- T-2 toxin, a prevalent mycotoxin, is linked to neurotoxicity.
- Microglial activation is implicated in T-2 toxin-induced neurological damage.
- The precise molecular mechanisms underlying this activation require further elucidation.
Purpose of the Study:
- To investigate the role of B cell translocation gene 2 (BTG2) in T-2 toxin-induced microglial activation.
- To explore the molecular pathways involved in T-2 toxin's effects on microglia.
Main Methods:
- High-throughput transcriptome sequencing to identify gene expression changes.
- Animal experiments to assess neurobehavioral effects and microglial activation.
- In vitro studies using microglia to examine BTG2 function and signaling pathways.
Main Results:
- T-2 toxin induced neurobehavioral deficits, increased microglial BTG2 expression, and promoted pro-inflammatory microglial activation.
- Minocycline, a microglial inhibitor, reversed these T-2 toxin-induced effects.
- Knockdown of BTG2 expression attenuated T-2 toxin-induced microglial activation.
- T-2 toxin activated the PI3K/AKT/NF-κB signaling pathway, a process reversed by BTG2 knockdown and inhibited by LY294002.
Conclusions:
- BTG2 is a key mediator in T-2 toxin-induced microglial activation.
- The PI3K/AKT/NF-κB signaling pathway is crucial for T-2 toxin's effects on microglia.
- BTG2 may exert its effects through the PI3K/AKT/NF-κB pathway.
