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Thyroid hormone suppresses the differentiation of osteoprogenitor cells to osteoblasts, but enhances functional activities of mature osteoblasts in cultured rat calvaria cells

✍ Scribed by Keiji Ohishi; Dr. Hiroshi Ishida; Toshihiko Nagata; Noriyuki Yamauchi; Dr. Chizuko Tsurumi; Seiji Nishikawa; Yoichi Wakano


Publisher
John Wiley and Sons
Year
1994
Tongue
English
Weight
1002 KB
Volume
161
Category
Article
ISSN
0021-9541

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✦ Synopsis


The effects of thyroid hormone on osteoblastic differentiation and activity were studied in fetal rat calvaria (RC) cells cultured for up to 30 days in medium supplemented with thyroid hormone-depleted serum. In this condition, the cells proliferated and differentiated to form mineralized bone nodules (BN) and expressed osteoblastic markers such as alkaline phosphatase (ALP), osteocalcin (OCN), and osteopontin (OPN). The continuous presence of triiodothyronine (T3) at 10-'-10-M in the medium inhibited the osteoblastic differentiation: 34% decrease in ALP activity on day 12 and 60% decrease in BN formation on day 15 at lo-" M. T3 at these doses had no effect on the DNA content of RC cells at confluence (day 6). Short-term (48-h) exposure of T3 at l o p 9 M or higher decreased ALP activity when RC cells were differentiating (days 7-1 1). However, when BN formation by the cells had already reached a plateau (day 28j, the activity was increased by treatment with T3 at 10-' -1 0-" M. OCN production was increased dose dependently by this treatment with T3 (2.1-fold and 1.3-fold of control at 1 0 ~-8 M on days 11 and 28, respectively). Similar increases were observed in the levels of OCN mRNA. In addition, increases in phosphorylated OPN in the medium (day 11) and mineralized matrix (day 28) were observed (1 ..?fold at 1 0-8-1 0-6 M), while OPN synthesis and the level of its mRNA were depressed by T3 (60-70% of control at M). These results suggest that T3 regulates osteoblastic differentiation and activity depending on the state of cell differentiation: T3 suppresses the differentiation of osteoprogenitor cells to osteoblasts, but enhances the functional activity of mature osteoblasts.