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Differential changes in GPR55 during microglial cell activation
Maciej Pietr1, Ewa Kozela, Rivka Levy
1Neurobiology Department, Weizmann Institute of Science, Rehovot 76100, Israel.
Abstract:
We examined how lipopolysaccharide (LPS) and interferon gamma (IFN-gamma), known to differentially activate microglia, affect the expression of G protein-coupled receptor 55 (GPR55), a novel cannabinoid receptor. We found that GPR55 mRNA is significantly expressed in both primary mouse microglia and the BV-2 mouse microglial cell line, and that LPS down-regulates this message. Conversely, IFN-gamma slightly decreases GPR55 mRNA in primary microglia, while it upregulates this message in BV-2 cells. Moreover, the GPR55 agonist, lysophosphatidylinositol, increases ERK phosphorylation in BV-2 stimulated with IFN-gamma, in correlation with the increased amount of GPR55 mRNA. Remarkably, these stimuli-induced changes in GPR55 expression are similar to those observed with CB(2)-R, suggesting that both receptors might be involved in neuroinflammation and that their expression is concomitantly controlled by the state of microglial activation.
Insights
Lipopolysaccharide (LPS) and interferon gamma (IFN-gamma) differentially regulate G protein-coupled receptor 55 (GPR55) expression in microglia. These findings suggest GPR55 and CB2 receptors are co-regulated during neuroinflammation.
Area of Science:
- Neuroscience
- Immunology
- Molecular Biology
Background:
- Microglia are key immune cells in the central nervous system.
- Microglial activation by lipopolysaccharide (LPS) and interferon gamma (IFN-gamma) plays a critical role in neuroinflammation.
- G protein-coupled receptor 55 (GPR55) is a putative cannabinoid receptor implicated in various physiological processes.
Purpose of the Study:
- To investigate the effects of LPS and IFN-gamma on GPR55 expression in microglia.
- To explore the functional consequences of altered GPR55 expression in activated microglia.
Main Methods:
- Quantitative real-time PCR was used to measure GPR55 mRNA levels in primary mouse microglia and BV-2 microglial cell line.
- Cells were stimulated with LPS and/or IFN-gamma.
- ERK phosphorylation was assessed using Western blotting in response to GPR55 activation.
Main Results:
- GPR55 mRNA was detected in both primary microglia and BV-2 cells.
- LPS significantly downregulated GPR55 mRNA expression.
- IFN-gamma differentially affected GPR55 mRNA levels, decreasing it in primary microglia but upregulating it in BV-2 cells.
- GPR55 activation led to increased ERK phosphorylation in IFN-gamma-stimulated BV-2 cells, correlating with elevated GPR55 mRNA.
Conclusions:
- Microglial activation state influences GPR55 expression.
- GPR55 and CB2 receptor expression patterns are similarly modulated by inflammatory stimuli.
- Both GPR55 and CB2 receptors may play a role in neuroinflammation and are coordinately regulated by microglial activation.
