This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Copyright Permission Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Isensee, J. Articles by Noppinger, P. R. Search for Related Content PubMed PubMed Citation Articles by Isensee, J. Articles by Noppinger, P. R. Pubmed/NCBI databases Gene GEO Profiles HomoloGene Protein UniGene Substance via MeSH

Expression Pattern of G Protein-Coupled Receptor 30 in LacZ Reporter Mice

Center for Cardiovascular Research and Berlin Institute for Gender in Medicine (J.I., L.M., V.Z., C.N., H.W., D.S., K.E., M.I., P.R.N.), Charité Universitätsmedizin, 10115 Berlin, Germany; German Mouse Clinic (H.F., V.G.-D., T.A., M.H.d.A.), Institute of Experimental Genetics, Helmholtz Zentrum München, German Research Center for Environmental Health, 85764 Munich/Neuherberg, Germany; Institute for Medical Microbiology, Immunology, and Hygiene (D.B., T.A.), Technische Universität München, 81675 München, Germany; Department of Experimental Genetics (M.H.d.A.), Center of Life and Food Sciences Weihenstephan, Technische Universität München, 85354 Freising, Germany; and Therapeutic Research Group Women’s Healthcare (C.O.), Bayer Schering Pharma AG, 13353 Berlin, Germany

Address all correspondence and requests for reprints to: Professor Dr. Patricia Ruiz Noppinger, Center for Cardiovascular Research, Charité Universitätsmedizin Berlin, Hessische Strasse 3-4, 10115 Berlin, Germany. E-mail: patricia.ruiz{at}charite.de.

Multiple reports implicated the function of G protein-coupled receptor (GPR)-30 with nongenomic effects of estrogen, suggesting that GPR30 might be a G-protein coupled estrogen receptor. However, the findings are controversial and the expression pattern of GPR30 on a cell type level as well as its function in vivo remains unclear. Therefore, the objective of this study was to identify cell types that express Gpr30 in vivo by analyzing a mutant mouse model that harbors a lacZ reporter (Gpr30-lacZ) in the Gpr30 locus leading to a partial deletion of the Gpr30 coding sequence. Using this strategy, we identified the following cell types expressing Gpr30: 1) an endothelial cell subpopulation in small arterial vessels of multiple tissues, 2) smooth muscle cells and pericytes in the brain, 3) gastric chief cells in the stomach, 4) neuronal subpopulations in the cortex as well as the polymorph layer of the dentate gyrus, 5) cell populations in the intermediate and anterior lobe of the pituitary gland, and 6) in the medulla of the adrenal gland. In further experiments, we aimed to decipher the function of Gpr30 by analyzing the phenotype of Gpr30-lacZ mice. The body weight as well as fat mass was unchanged in Gpr30-lacZ mice, even if fed with a high-fat diet. Flow cytometric analysis revealed lower frequencies of T cells in both sexes of Gpr30-lacZ mice. Within the T-cell cluster, the amount of CD62L-expressing cells was clearly reduced, suggesting an impaired production of T cells in the thymus of Gpr30-lacZ mice.

This article has been cited by other articles:

				S. Liu, C. Le May, W. P.S. Wong, R. D. Ward, D. J. Clegg, M. Marcelli, K. S. Korach, and F. Mauvais-Jarvis Importance of Extranuclear Estrogen Receptor-{alpha} and Membrane G Protein-Coupled Estrogen Receptor in Pancreatic Islet Survival Diabetes, October 1, 2009; 58(10): 2292 - 2302. [Abstract] [Full Text] [PDF]

				G. G J Hazell, S. T Yao, J. A Roper, E. R Prossnitz, A.-M. O'Carroll, and S. J Lolait Localisation of GPR30, a novel G protein-coupled oestrogen receptor, suggests multiple functions in rodent brain and peripheral tissues J. Endocrinol., August 1, 2009; 202(2): 223 - 236. [Abstract] [Full Text] [PDF]

				E. R. Levin G Protein-Coupled Receptor 30: Estrogen Receptor or Collaborator? Endocrinology, April 1, 2009; 150(4): 1563 - 1565. [Full Text] [PDF]