cineurin/NFATc activity experience bone loss, Winslow, Crabtree, and their colleagues wanted to see whether this pathway would be important in bone development and function as well. They studied mutant mice in which the NFATc1 in osteoblasts had been modified so that it could move more easily to the nucleus and become a little more active than usual.
Mice with the hyperactive NFATc in their osteoblasts had an immense increase in bone mass compared to normal mice, suggesting that the balance between bone formation and breakdown had tipped.
When the researchers examined the cells in these mice, they found that up-regulating NFATc signaling in osteoblasts increased the numbers of both types of bone cells. ‘It was clear that increased NFATc activity in osteoblasts influenced both osteoblasts and osteoclasts,’ Winslow said.
The researchers found that mice that showed enhanced NFATc activity in their osteoblasts had many more of these bone-forming cells, which explained the increase in bone mass. They also found a possible explanation for why there were more bone-destroying osteoclasts. Osteoblasts with hyperactive NFATc expressed higher levels of inflammatory proteins called chemokines, which promote osteoclast development.
‘Osteoblasts produce factors that recruit the progenitors of osteoclasts, and so when osteoblast numbers go up, osteoclast numbers go up,’ Crabtree said. This link between osteoblast and osteoclast numbers explains in part how the two types of cells normally stay balanced in animals, he added.
Mice with abnormally active NFATc probably develop so much bone mass because this delicate balance between osteoblasts and osteoclasts has been altered, Crabtree suggested. In the mutant mice, ‘there's also a huge increase in osteoclasts, but they never catch up,’ he said. ‘The balance has been tipped.’
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