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Published on: December 11, 2020
1-O-alkyl glycerophosphate-induced CD36 expression drives oxidative stress in microglial cells
1Department of Pharmacology and Therapeutic Innovation, Nagasaki University Graduate School of Biomedical Sciences, 1-14 Bunkyo-machi, Nagasaki, 852-8521 Japan.
Abstract:
Microglia, the tissue-resident macrophages in the central nervous system, are important for the initiation and perpetuation of neuroinflammation. Peroxisome proliferator-activated receptor gamma (PPARγ) is a ligand-inducible transcription factor and plays an important role in fatty acid metabolism. Our previous study found that 1-O-alkyl glycerophosphate (AGP), a naturally occurring ether analog of lysophosphatidic acid, is a high-affinity, partial agonist of PPARγ. In this study, we investigated the role of AGP in microglial activation and illustrated the underlying molecular mechanism. We found that AGP treatment increased the production of intracellular reactive oxygen species and induced PPARγ activation in microglial cells. Interestingly, AGP also up-regulated the expression levels of the cluster of differentiation 36 (CD36) scavenger receptor, a high-affinity receptor for oxidized low-density lipoproteins. The findings suggest that AGP induces PPARγ activation, enhances CD36 expression and increases the production of intracellular reactive oxygen species (ROS) in microglial cells.
Insights
1-O-alkyl glycerophosphate (AGP) activates peroxisome proliferator-activated receptor gamma (PPARγ) in microglia. This activation enhances cluster of differentiation 36 (CD36) expression and increases reactive oxygen species (ROS) production.
Area of Science:
- Neuroimmunology
- Cellular and Molecular Neuroscience
- Inflammation Research
Background:
- Microglia are central nervous system macrophages crucial for neuroinflammation.
- Peroxisome proliferator-activated receptor gamma (PPARγ) regulates fatty acid metabolism and immune responses.
- 1-O-alkyl glycerophosphate (AGP) is a high-affinity, partial agonist of PPARγ.
Purpose of the Study:
- To investigate the role of AGP in microglial activation.
- To elucidate the molecular mechanisms underlying AGP's effects on microglia.
Main Methods:
- Treatment of microglial cells with AGP.
- Measurement of intracellular reactive oxygen species (ROS) production.
- Assessment of PPARγ activation and cluster of differentiation 36 (CD36) expression levels.
Main Results:
- AGP treatment increased intracellular ROS production in microglial cells.
- AGP induced PPARγ activation within microglial cells.
- AGP up-regulated the expression of the CD36 scavenger receptor.
Conclusions:
- AGP modulates microglial activation through PPARγ-dependent pathways.
- AGP enhances CD36 expression and ROS production in microglia.
- These findings provide insights into AGP's potential role in neuroinflammatory processes.
