MODULATION OF OSTEOBLAST BEHAVIOR BY TENASCIN

The extracellular matrix protein tenascin is secreted by osteoblasts b ut absent from mineralized bone matrix. The current study was undertak en to test the hypothesis that tenascin regulates osteoblast behaviour . Three osteoblastlike cell lines UMR-106, ROS-17/2.8 (rat) and SAOS-2 (human) were used to investigate the role of tenascin in osteoblast m orphology, differentiation and proliferation. Two of three cell lines adhered specifically to tenascin, remaining round and failing to sprea d. Tenascin as a substratum stimulated alkaline phosphatase activity ( a marker of osteoblast differentiation) in two of three cell lines. Mo reover, anti-tenascin in the medium caused a reduction in alkaline pho sphatase levels in all three cell lines. Antitenascin also inhibited c ollagen synthesis, an important osteoblast function. Since it seemed p ossible that tenascin may exert its effects on cell function through i ts ability to cause cell rounding, the ability of cell shape change al one to influence alkaline phosphatase levels was investigated. Cells w ere incubated in the presence of cytochalasin D and alkaline phosphata se levels assayed. Alkaline phosphatase activity was not elevated by c ytochalasin D treatment, indicating that cell rounding alone is insuff icient to mimic the effect of tenascin. Anti-tenascin caused a slight increase in proliferation of SAOS-2 cells, indicating that tenascin is itself inhibitory. In ROS 17/2.8 and UMR-106 cells, in contrast, prol iferation was inhibited by anti-tenascin. The results presented here i ndicate that tenascin is able to stimulate osteoblastic differentiatio n and that endogenous tenascin helps to maintain the functional state of cultured osteoblast-like cells.