| First Author | Guo J | Year | 2002 |
| Journal | Dev Cell | Volume | 3 |
| Issue | 2 | Pages | 183-94 |
| PubMed ID | 12194850 | Mgi Jnum | J:108984 |
| Mgi Id | MGI:3625556 | Doi | 10.1016/s1534-5807(02)00218-6 |
| Citation | Guo J, et al. (2002) The PTH/PTHrP receptor can delay chondrocyte hypertrophy in vivo without activating phospholipase C. Dev Cell 3(2):183-94 |
| abstractText | One G protein-coupled receptor (GPCR) can activate more than one G protein, but the physiologic importance of such activation has not been demonstrated in vivo. We have generated mice expressing exclusively a mutant form of the PTH/PTHrP receptor (DSEL) that activates adenylyl cyclase normally but not phospholipase C (PLC). DSEL mutant mice exhibit abnormalities in embryonic endochondral bone development, including delayed ossification and increased chondrocyte proliferation. Analysis of the differentiation of embryonic metatarsals in vitro shows that PTH(1-34) and forskolin inhibit, whereas active phorbol ester stimulates, hypertrophic differentiation. Thus, PLC signaling via the PTH/PTHrP receptor normally slows the proliferation and hastens the differentiation of chondrocytes, actions that oppose the dominant effects of PTH/PTHrP receptors and that involve cAMP-dependent signaling pathways. |
