Stimulation of alkaline phosphatase activity in cultured neonatal mouse calvarial bone cells by parathyroid hormone

1985 ◽  
Vol 37 (5) ◽  
pp. 530-538 ◽  
Author(s):  
John A. Yee
1996 ◽  
Vol 41 (1) ◽  
pp. 41-45 ◽  
Author(s):  
Yoshitaka Yoshimura ◽  
Yoh Hisada ◽  
Kuniaki Suzuki ◽  
Yoshiaki Deyama ◽  
Akira Matsumoto

1995 ◽  
Vol 67 ◽  
pp. 241
Author(s):  
Yoshitaka Yoshimura ◽  
Yoh Hisada ◽  
Kuniaki Suzuki ◽  
Yosbiaki Deyama ◽  
Akira Matsumoto

1991 ◽  
Vol 69 (2-3) ◽  
pp. 132-140 ◽  
Author(s):  
Rebecca Ber ◽  
Takao Kubota ◽  
Jaro Sodek ◽  
Jane E. Aubin

Although transforming growth factor-β (TGF-β) has been implicated in the local regulation of bone growth and remodelling, its specific effects on different subpopulations of bone cells have not been elucidated. Cells derived from bone are known to be heterogeneous and include both cells of different lineages and osteoblastic populations with different levels of expression of osteoblast-associated properties. Consequently, we have isolated clonal populations of bone cells to examine more precisely the effects of TGF-β on individual subpopulations. Several clonal populations were isolated by limiting dilution from cells derived from 21-day-old fetal rat calvaria. Two of these clones, RCA 11 and RCB 2, were used here. While the two clones responded similarly to parathyroid hormone (PTH) and isoproterenol (ISP) with increases in intracellular cAMP, prostaglandin E2 (PGE2) elicited a 10-fold higher response in RCB 2 cells compared with RCA 11. RCB 2 cells expressed a 10-fold higher alkaline phosphatase activity compared with RCA 11. Both clones synthesized a variety of bone matrix associated proteins, but only RCA 11 synthesized SPP-1 (osteopontin) constitutively. TGF-β stimulated growth of RCB 2 cells after 24 and 48 h of treatment, but had no effect on growth of RCA 11. TGF-β supported anchorage-independent growth of RCB 2 cells, but not that of RCA 11. A 24-h exposure to TGF-β decreased cAMP responsiveness to PTH and ISP slightly in both clones, but had no effect on PGE2 responses. Significant reductions in alkaline phosphatase activity were seen in both clones after 24- and 48-h treatments with TGF-β. Total protein synthesis as measured by [35S]methionine incorporation was stimulated significantly in both clones, but TGF-β selectively stimulated type I collagen compared with type III collagen. SPARC (osteonectin) and secreted phosphoprotein 1 (SPP-1; osteopontin) were stimulated by TGF-β in both RCA 11 and RCB 2 cells. These results indicate that individual clonal populations of cells within bone may be modulated differentially by TGF-β.Key words: transforming growth factor-β, osteoblasts, clonal cell lines, matrix synthesis.


1986 ◽  
Vol 111 (2) ◽  
pp. 285-288 ◽  
Author(s):  
Masayoshi Yamaguchi ◽  
Teruyuki Sakashita

Abstract. The interaction of vitamin D3 and zinc on bone metabolism was investigated in the femur of weanling rats. Oral administration of vitamin D3 (1.0 μg/100 g body weight) did not cause any increase in the zinc accumulation in the femoral tissue following treatment with zinc sulphate (1.0 mg Zn/100 g). Administration of vitamin D3 or zinc produced significant increases the alkaline phosphatase activity and DNA content of the femoral diaphvsis but not of the epiphysis. The increase in alkaline phosphatase activity was enhanced additionally by simultaneous administration of vitamin D3 and zinc. Moreover, the increase in DNA content was enhanced markedly (about 4 times) by these treatments. At a dose of 0.5 μg of vitamin D3 per 100 g, DNA content was at the control level. This level was increased about 2 times by simultaneous administration of zinc (1.0 mg/100 g). The increase in alkaline phosphatase activity following simultaneous administration of vitamin D3 and zinc was significantly inhibited by treatment with cycloheximide, actinomycin D, or mitomycin C. Also, the increase in DNA content was completely inhibited by mitomycin C treatment. The present data suggest that the combination of vitamin D3 and zinc has a multiple effect on the stimulation of bone growth and mineralization in weanling rats, and that this effect is based on a stimulation of the DNA synthesis in bone cells.


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