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Publication : The G-protein-coupled receptor GPR103 regulates bone formation.

First Author  Baribault H Year  2006
Journal  Mol Cell Biol Volume  26
Issue  2 Pages  709-17
PubMed ID  16382160 Mgi Jnum  J:144011
Mgi Id  MGI:3829586 Doi  10.1128/MCB.26.2.709-717.2006
Citation  Baribault H, et al. (2006) The G-protein-coupled receptor GPR103 regulates bone formation. Mol Cell Biol 26(2):709-17
abstractText  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.
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