Differential changes in GPR55 during microglial cell activation

Maciej Pietr; Ewa Kozela; Rivka Levy; Neta Rimmerman; Yi Hsing Lin; Nephi Stella; Zvi Vogel; Ana Juknat

doi:10.1016/j.febslet.2009.05.028

Differential changes in GPR55 during microglial cell activation

Maciej Pietr, Ewa Kozela, Rivka Levy, Neta Rimmerman, Yi Hsing Lin, Nephi Stella, Zvi Vogel^*, Ana Juknat

^*Corresponding author for this work

Research output: Contribution to journal › Article › peer-review

110 Scopus citations

Abstract

We examined how lipopolysaccharide (LPS) and interferon gamma (IFN-γ), 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-γ 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-γ, in correlation with the increased amount of GPR55 mRNA. Remarkably, these stimuli-induced changes in GPR55 expression are similar to those observed with CB₂-R, suggesting that both receptors might be involved in neuroinflammation and that their expression is concomitantly controlled by the state of microglial activation.

Original language	English
Pages (from-to)	2071-2076
Number of pages	6
Journal	FEBS Letters
Volume	583
Issue number	12
DOIs	https://doi.org/10.1016/j.febslet.2009.05.028
State	Published - 18 Jun 2009
Externally published	Yes

Bibliographical note

Funding Information:
This work was supported by the Dr. Miriam and Sheldon G. Adelson Program for Nerve Regeneration and Repair, the Nella and Leon Benoziyo Center for Neurosciences and the Israeli Ministry of Health (Z.V.) and by NIDA (N. S.). A.J. is supported by the Israeli Ministry of Absorption.

Keywords

CB receptor
Cannabinoid
ERK phosphorylation
G protein-coupled receptor 55
Interferon gamma
Lipopolysaccharide
Lysophosphatidylinositol
Microglia

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1016/j.febslet.2009.05.028

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title = "Differential changes in GPR55 during microglial cell activation",

abstract = "We examined how lipopolysaccharide (LPS) and interferon gamma (IFN-γ), 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-γ 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-γ, in correlation with the increased amount of GPR55 mRNA. Remarkably, these stimuli-induced changes in GPR55 expression are similar to those observed with CB2-R, suggesting that both receptors might be involved in neuroinflammation and that their expression is concomitantly controlled by the state of microglial activation.",

keywords = "CB receptor, Cannabinoid, ERK phosphorylation, G protein-coupled receptor 55, Interferon gamma, Lipopolysaccharide, Lysophosphatidylinositol, Microglia",

author = "Maciej Pietr and Ewa Kozela and Rivka Levy and Neta Rimmerman and Lin, {Yi Hsing} and Nephi Stella and Zvi Vogel and Ana Juknat",

note = "Funding Information: This work was supported by the Dr. Miriam and Sheldon G. Adelson Program for Nerve Regeneration and Repair, the Nella and Leon Benoziyo Center for Neurosciences and the Israeli Ministry of Health (Z.V.) and by NIDA (N. S.). A.J. is supported by the Israeli Ministry of Absorption.",

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AU - Pietr, Maciej

AU - Kozela, Ewa

AU - Levy, Rivka

AU - Rimmerman, Neta

AU - Lin, Yi Hsing

AU - Stella, Nephi

AU - Vogel, Zvi

AU - Juknat, Ana

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PY - 2009/6/18

Y1 - 2009/6/18

N2 - We examined how lipopolysaccharide (LPS) and interferon gamma (IFN-γ), 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-γ 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-γ, in correlation with the increased amount of GPR55 mRNA. Remarkably, these stimuli-induced changes in GPR55 expression are similar to those observed with CB2-R, suggesting that both receptors might be involved in neuroinflammation and that their expression is concomitantly controlled by the state of microglial activation.

AB - We examined how lipopolysaccharide (LPS) and interferon gamma (IFN-γ), 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-γ 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-γ, in correlation with the increased amount of GPR55 mRNA. Remarkably, these stimuli-induced changes in GPR55 expression are similar to those observed with CB2-R, suggesting that both receptors might be involved in neuroinflammation and that their expression is concomitantly controlled by the state of microglial activation.

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KW - ERK phosphorylation

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KW - Interferon gamma

KW - Lipopolysaccharide

KW - Lysophosphatidylinositol

KW - Microglia

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Differential changes in GPR55 during microglial cell activation

Abstract

Bibliographical note

Keywords

UN SDGs

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