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Molecular and Cellular Biology, January 2006, p. 709-717, Vol. 26, No. 2
0270-7306/06/$08.00+0     doi:10.1128/MCB.26.2.709-717.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

The G-Protein-Coupled Receptor GPR103 Regulates Bone Formation

Helene Baribault,1* Jean Danao,1 Jamila Gupte,1 Li Yang,1 Banghua Sun,2 William Richards,2 and Hui Tian1

Department of Biology Research, Amgen, South San Francisco, California 94080,1 Department of Metabolic Disorders, Amgen, Thousand Oaks, California 913202

Received 25 August 2005/ Accepted 30 September 2005

GPR103 is a G-protein-coupled receptor with reported expression in brain, heart, kidney, adrenal gland, retina, and testis. It encodes a 455-amino-acid protein homologous to neuropeptide FF2, neuropeptide Y2, and galanin GalR1 receptors. Its natural ligand was recently identified as 26RFa, a novel human RF-amide-related peptide with orexigenic activity. To identify the function of GPR103, we generated GPR103-deficient mice. Homozygous mutant mice were viable and fertile. Their body weight was undistinguishable from that of their wild-type littermates. Histological analysis revealed that GPR103–/– mice exhibited a thinned osteochondral growth plate, a thickening of trabecular branches, and a reduction in osteoclast number, suggestive of an early arrest of osteochondral bone formation. Microcomputed tomography confirmed the reduction in trabecular bone and connective tissue densities in GPR103 knockout animals. Whole-body radiography followed by morphometric analysis revealed a kyphosis in mutant animals. Reverse transcription-PCR analysis showed that GPR103 was expressed in human skull, mouse spine, and several osteoblast cell lines. Dexamethasone, a known inhibitor of osteoblast growth and inducer of osteoblast differentiation, inhibited GPR103 expression in human osteoblast primary cultures. Altogether, these results suggest that osteopenia in GPR103–/– mice may be mediated directly by the loss of GPR103 expression in bone.

* Corresponding author. Mailing address: Amgen, Mail Stop ASF1-1, 1120 Veterans Blvd., South San Francisco, CA 94080. Phone: (650) 244-2067. Fax: (650) 244-2392. E-mail: helene{at}amgen.com.

Molecular and Cellular Biology, January 2006, p. 709-717, Vol. 26, No. 2
0022-538X/06/$08.00+0     doi:10.1128/MCB.26.2.709-717.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



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