Exogenous prostacyclin, but not prostaglandin E sub(2), produces similar responses in both G6PD activity and RNA production as mechanical loading, and increases IGF-II release, in adult cancellous bone in culture

• Published in: Calcified tissue international 1993-01, Vol.53 (5), p.324-329
• Main Authors: Rawlinson, SCF, Mohan, S, Baylink, D J, Lanyon, LE
• Format: Article
• Language: English
• ISSN: 0171-967X

Cyclic mechanical loading in vivo that leads to new bone formation is also associated in osteocytes and surface bone cells with almost immediate increases in G6PD activity, and later increases in RNA production. Both these early, loading-related, responses can be reproduced in organ culture of adult cancellous bone, and both are abolished by the presence of indomethacin in the culture medium at the time of loading. The implication that prostaglandins (PGs) are involved in the control of loading-related osteogenesis is supported by increases in prostacyclin (PGI sub(2)) and PGE sub(2) release from cores of cancellous bone during loading. In the experiments reported here, PGE sub(2) and PGI sub(2) were added exogenously (10 super(-6) M) to perfusable cores of adult canine cancellous bone to determine whether they would simulate the loading-related responses in G6PD activity and RNA synthesis. PGE sub(2) increased G6PD activity in surface cells and osteocytes within 8 minutes but had no effect on [ super(3)H]-uridine incorporation at 6 hours. PGI sub(2) stimulated both G6PD activity and [ super(3)H]-uridine incorporation equally in osteocytes and surface cells. Neither PG produced any significant change in medium concentrations of IGF-I, and PGE sub(2) had no effect on IGF-II. In contrast, PGI sub(2) elevated the medium concentration of IGF-II threefold. IGF-I and IGF-II were localized immunocytochemically to osteocytes and surface cells in both treated and untreated cores. Prostacyclin, but not PGE sub(2), appears to imitate the early loading-related increases in G6PD activity and RNA synthesis in bone cells in situ. Prostacyclin, but not PGE sub(2), also stimulates the early release of IGF-II.