Abstract
Parathyroid hormone (PTH) is an anabolic agent that mediates bone formation through activation of the Gαs-, Gαq- and β-arrestin-coupled parathyroid hormone receptor type 1 (PTH1R). Pharmacological evidence based on the effect of PTH(7–34), a PTH derivative that is said to preferentially activate β-arrestin signaling through PTH1R, suggests that PTH1R-activated β-arrestin signaling mediates anabolic effects on bone. Here, we performed a thorough evaluation of PTH(7–34) signaling behaviour using quantitative assays for β-arrestin recruitment, Gαs- and Gαq-signaling. We found that PTH(7–34) inhibited PTH-induced cAMP accumulation, but was unable to induce β-arrestin recruitment, PTH1R internalization and ERK1/2 phosphorylation in HEK293, CHO and U2OS cells. Thus, the β-arrestin bias of PTH(7–34) is not apparent in every cell type examined, suggesting that correlating in vivo effects of PTH(7–34) to in vitro pharmacology should be done with caution.
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