Effects of a synthetic N-terminal fragment of stanniocalcin on the metabolism of mammalian bone in vitro.

Abstract A synthetic peptide corresponding to the N-terminal amino acid residues of stanniocalcin (STC1–20) and including a region that is known to be an active site in teleosts was prepared and tested for its effects on the metabolism of mammalian bone in vitro. (10 −10 −10 −12 M) inhibited increases in the number of tartrate-resistant acid phosphatase-positive, multinucleated cells promoted by an N-terminal fragment of human parathyroid hormone (hPTH1–34) in cultures of murine hemopoietic cells. STC1–20 also slightly decreased the rate of loss of radioactivity from calvariae of fetal rats that had been prelabeled with 45 Ca, both with and without stimulation by hPTH1–34. The accumulation of cAMP induced by hPTH1–34 in ROS 17/2. cells was suppressed by(10 −10 −10 −12 M). Treatment with (10 −11 −10 −13 M) caused increases of the rate of incorporation of [ 3 H]proline into the collagenase-digestible protein of calvariae in newborn mice. From these results, it appears that STC1–20 has diverse effects on the metabolism of mammalian bone, causing a biphasic response. Such effects have not been observed with intact stanniocalcin or with materials from the corpuscles of Stannius and they are also different from the effects of hPTH1–34.