Abstract
Transforming growth factor .beta. (TGF-.beta.) is produced by bone cells, is abundant in bone matrix, and regulates bone cell biochemical processes. In osteoblast-enriched fetal rat parietal bone cell cultures, low TGF-.beta. doses increase DNA synthesis, whereas higher levels are less mitogenic, stimulate collagen production and decrease alkaline phosphatase activity. Parathyroid hormone by itself has minimal effects on these processes, but it opposes the effects of TGF-.beta. and alters TGF-.beta. binding to its receptors in osteoblast-enriched cultures. Some functions ascribed to parathyroid hormone in bone may therefore result from alterations in TGF-.beta. activity, suggesting that the local effects of TGF-.beta. in bone are under systemic hormonal control.