Expression analysis of G Protein-Coupled Receptors in mouse macrophages

Jane E Lattin¹ , Kate Schroder¹ , Andrew I Su² , John R Walker² , Jie Zhang² , Tim Wiltshire² , Kaoru Saijo³ , Christopher K Glass³ , David A Hume⁴ , Stuart Kellie¹^,5 and Matthew J Sweet¹^,5

¹Cooperative Research Centre for Chronic Inflammatory Diseases and Special Research Centre for Functional and Applied Genomics, Institute for Molecular Bioscience, Institute for Molecular Bioscience, University of Queensland, Brisbane, Queensland, 4072, Australia

²The Genomics Institute of the Novartis Research Foundation, San Diego, CA 92121, USA

³The Department of Cellular and Molecular Medicine, University of California, San Diego, La Jolla, CA 92093-0651, USA

⁴The Roslin Institute, University of Edinburgh, Roslin EH25 9PS, Scotland, UK

⁵School of Molecular and Microbial Sciences, University of Queensland, Brisbane, Queensland, 4072, Australia

author email corresponding author email

Immunome Research 2008, 4:5doi:10.1186/1745-7580-4-5


Published:	29 April 2008

Abstract

Background

Monocytes and macrophages express an extensive repertoire of G Protein-Coupled Receptors (GPCRs) that regulate inflammation and immunity. In this study we performed a systematic micro-array analysis of GPCR expression in primary mouse macrophages to identify family members that are either enriched in macrophages compared to a panel of other cell types, or are regulated by an inflammatory stimulus, the bacterial product lipopolysaccharide (LPS).

Results

Several members of the P2RY family had striking expression patterns in macrophages; P2ry6 mRNA was essentially expressed in a macrophage-specific fashion, whilst P2ry1 and P2ry5 mRNA levels were strongly down-regulated by LPS. Expression of several other GPCRs was either restricted to macrophages (e.g. Gpr84) or to both macrophages and neural tissues (e.g. P2ry12, Gpr85). The GPCR repertoire expressed by bone marrow-derived macrophages and thioglycollate-elicited peritoneal macrophages had some commonality, but there were also several GPCRs preferentially expressed by either cell population.

Conclusion

The constitutive or regulated expression in macrophages of several GPCRs identified in this study has not previously been described. Future studies on such GPCRs and their agonists are likely to provide important insights into macrophage biology, as well as novel inflammatory pathways that could be future targets for drug discovery.