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Research ArticleArticle

Cultured Rat Microglial Cells Synthesize the Endocannabinoid 2-Arachidonylglycerol, Which Increases Proliferation via a CB2 Receptor-Dependent Mechanism

Erica J. Carrier, Christopher S. Kearn, Andrew J. Barkmeier, Nicole M. Breese, Wenqi Yang, Kasem Nithipatikom, Sandra L. Pfister, William B. Campbell and Cecilia J. Hillard
Molecular Pharmacology April 2004, 65 (4) 999-1007; DOI: https://doi.org/10.1124/mol.65.4.999
Erica J. Carrier
Department of Pharmacology and Toxicology, Medical College of Wisconsin, Milwaukee, Wisconsin
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Christopher S. Kearn
Department of Pharmacology and Toxicology, Medical College of Wisconsin, Milwaukee, Wisconsin
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Andrew J. Barkmeier
Department of Pharmacology and Toxicology, Medical College of Wisconsin, Milwaukee, Wisconsin
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Nicole M. Breese
Department of Pharmacology and Toxicology, Medical College of Wisconsin, Milwaukee, Wisconsin
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Wenqi Yang
Department of Pharmacology and Toxicology, Medical College of Wisconsin, Milwaukee, Wisconsin
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Kasem Nithipatikom
Department of Pharmacology and Toxicology, Medical College of Wisconsin, Milwaukee, Wisconsin
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Sandra L. Pfister
Department of Pharmacology and Toxicology, Medical College of Wisconsin, Milwaukee, Wisconsin
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William B. Campbell
Department of Pharmacology and Toxicology, Medical College of Wisconsin, Milwaukee, Wisconsin
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Cecilia J. Hillard
Department of Pharmacology and Toxicology, Medical College of Wisconsin, Milwaukee, Wisconsin
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Abstract

Microglia, as phagocytes and antigen-presenting cells in the central nervous system, are activated in such disease processes as stroke and multiple sclerosis. Because peripheral macrophages are capable of producing endocannabinoids, we have examined endocannabinoid production in a macrophage-colony stimulating factor (M-CSF)-dependent rat microglial cell line (RTMGL1) using reversed phase high-pressure liquid chromatography and liquid chromatography-mass spectroscopy. We determined that cultured microglial cells produce the endocannabinoid 2-arachidonylglycerol (2-AG) as well as anandamide in smaller quantities. When 2-AG, but not anandamide, is added exogenously, RTMGL1 microglia increase their proliferation. This increased proliferation is blocked by an antagonist of the CB2 receptor N-[(1S)endo-1,3,3-trimethyl bicyclo heptan-2-yl]-5-(4-chloro-3-methylphenyl)-1-(4-methylbenzyl)-pyrazole-3-carboxamide (SR144528) and mimicked by the CB2 receptor-specific agonist 1,1-dimethylbutyl-1-deoxy-Δ9-tetrahydrocannabinol (JWH133). Accompanying the increase in proliferation seen with 2-AG is an increase in active ERK1 that is also blocked with SR144528. The RTMGL1 microglial cells, which exist in a primed state, express the CB1 and CB2 receptors as demonstrated by reverse transcription-polymerase chain reaction and immunostaining. The CB2 receptor in untreated cells is expressed both at the cell surface and internally, and exposure of the cells to 2-AG significantly increases receptor internalization. These data suggest that 2-AG activation of CB2 receptors may contribute to the proliferative response of microglial cells, as occurs in neurodegenerative disorders.

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Molecular Pharmacology: 65 (4)
Molecular Pharmacology
Vol. 65, Issue 4
1 Apr 2004
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Research ArticleArticle

Cultured Rat Microglial Cells Synthesize the Endocannabinoid 2-Arachidonylglycerol, Which Increases Proliferation via a CB2 Receptor-Dependent Mechanism

Erica J. Carrier, Christopher S. Kearn, Andrew J. Barkmeier, Nicole M. Breese, Wenqi Yang, Kasem Nithipatikom, Sandra L. Pfister, William B. Campbell and Cecilia J. Hillard
Molecular Pharmacology April 1, 2004, 65 (4) 999-1007; DOI: https://doi.org/10.1124/mol.65.4.999

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Research ArticleArticle

Cultured Rat Microglial Cells Synthesize the Endocannabinoid 2-Arachidonylglycerol, Which Increases Proliferation via a CB2 Receptor-Dependent Mechanism

Erica J. Carrier, Christopher S. Kearn, Andrew J. Barkmeier, Nicole M. Breese, Wenqi Yang, Kasem Nithipatikom, Sandra L. Pfister, William B. Campbell and Cecilia J. Hillard
Molecular Pharmacology April 1, 2004, 65 (4) 999-1007; DOI: https://doi.org/10.1124/mol.65.4.999
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