| First Author | Kawamata Y | Year | 2003 |
| Journal | J Biol Chem | Volume | 278 |
| Issue | 11 | Pages | 9435-40 |
| PubMed ID | 12524422 | Mgi Jnum | J:82367 |
| Mgi Id | MGI:2652648 | Doi | 10.1074/jbc.M209706200 |
| Citation | Kawamata Y, et al. (2003) A G Protein-coupled Receptor Responsive to Bile Acids. J Biol Chem 278(11):9435-40 |
| abstractText | So far some nuclear receptors for bile acids have been identified. However, no cell surface receptor for bile acids has yet been reported. We found that a novel G protein-coupled receptor, TGR5, is responsive to bile acids as a cell-surface receptor. Bile acids specifically induced receptor internalization, the activation of extracellular signal-regulated kinase mitogen-activated protein kinase, the increase of guanosine 5'-O-3-thio-triphosphate binding in membrane fractions, and intracellular cAMP production in Chinese hamster ovary cells expressing TGR5. Our quantitative analyses for TGR5 mRNA showed that it was abundantly expressed in monocytes/macrophages in human and rabbit. Treatment with bile acids was found to suppress the functions of rabbit alveolar macrophages including phagocytosis and lipopolysaccharide-stimulated cytokine productions. We prepared a monocytic cell line expressing TGR5 by transfecting a TGR5 cDNA into THP-1 cells that did not express TGR5 originally. Treatment with bile acids suppressed the cytokine productions in the THP-1 cells expressing TGR5, whereas it did not influence those in the original THP-1 cells, suggesting that TGR5 is implicated in the suppression of macrophage functions by bile acids. |
