Regulation of Plasminogen Activator Production by Bone-Resorbing Hormones in Normal and Malignant Osteoblasts*

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Abstract
The plasminogen activator (PA) activity of clonal rat osteogenic sarcoma cell (phenotypically osteoblast) and of osteoblast-rich rat calvarial cells is shown to be increased by treatment with the bone-resorbing hormones, PTH [parathyroid hormone], 1,25-dihydroxyvitamin D3, prostaglandin E2 and epidermal growth factor. Dose-dependent increases were observed, after a lag period of 4-8 h. Stimulated and control PA activities were inhibited by actinomycin D and cycloheximide, but not by cytosine arabinoside. Glucocorticoid hormones prevented the hormone stimulation, but other steroids did not. Calcitonin had no effect either on basal or on hormone-treated PA activity. Isobutyl-methylxanthine alone increased PA activity, and enchanced responsiveness to PTH and to prostaglandin E2. These data point to a common pathway in the actions upon osteoblasts of several hormones with diverse initial cellular actions and raise the possibility that the PA/plasmin system may contribute to cellular mechanisms of bone turnover.