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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 
 
 

Effect of transforming growth factor beta on parathyroid hormone receptor binding and cAMP formation in rat osteosarcoma cells.

Transforming growth factor beta (TGF-beta) is now recognized as an important growth regulator and modulator in bone, where it apparently acts in an autocrine or paracrine fashion. In an effort to help elucidate how TGF-beta may interact with parathyroid hormone ( PTH) to influence bone turnover, we examined the idea that TGF-beta might alter the number or affinity of PTH receptors in osteoblastic bone cells, PTH receptor binding was assessed in cultured ROS 17/2.8 cells using [125I]PTHrP-(1-34) as labeled ligand. Specific binding to intact cells was measured in the presence of up to 1 microM unlabeled rPTH-(1-34), and cAMP in cell extracts was determined by RIA. Incubation of ROS cells with 2 ng/ml of TGF-beta for the maximally effective time of 3 days increased the number of PTH binding sites (Bmax) by 47 +/- 13%, with no change in the KD (3 nM). TGF-beta also increased the intracellular cAMP response to 0.3 nM rPTH-(1-34) (ED50) by 53 +/- 22%. Both effects were dose dependent, with 1-4 ng/ml of TGF-beta producing maximal effects, and both effects were blocked by the protein synthesis inhibitor cycloheximide (2-5 microM). Since TGF-beta induced comparable increases in both PTH binding and cAMP formation, the findings suggest that TGF-beta can increase the number of functional PTH receptors in cultured ROS 17/2.8 cells. This effect may reflect an action of TGF-beta to slow replication and promote differentiated functions in these cells.[1]

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