Increasing the activity of a protein called NFATc1 tends to cause massive bone accumulation that target the drugs used to treat osteoporosis //- HHMI investigator Gerald Crabtree and HHMI predoctoral fellow Monte Winslow reports.
In vertebrates, bone is constantly being formed and being broken down throughout life. Cells called osteoclasts continuously degrade bone, while cells called osteoblasts replenish it.
‘Ideally, they are perfectly balanced,’ said Crabtree, the senior author of the study. ‘Over the course of a lifetime, if everything goes well, we'll maintain almost exactly identical bone mass.’ However, if the balance is upset, and more bone is destroyed than formed, osteoporosis results, increasing the risk of fractures.
The new study arose from the researchers' curiosity about reports that patients who were treated with the drug cyclosporine – often given to suppress the immune system before organ transplants – tended to lose bone mass. Those patients were also at increased risk of bone fractures, said first author Winslow, who led the study as an HHMI predoctoral fellow in Crabtree's lab. Winslow is now working as a postdoctoral fellow in the lab of HHMI investigator Tyler Jacks at the Massachusetts Institute of Technology.
Cyclosporine inhibits a signaling protein complex known as calcineurin, which chemically modifies the NFATc family of proteins. This modification changes its shape. With its new shape, NFATc can move into the nucleus of the cell, where it can trigger the activation of many genes. Although initially shown to regulate immune cell function, NFATc also functions in other cells to regulate heart development, blood vessel formation, neural development and function, and muscle development. Its function seems to depend on the time and place of its activation, like a context-sensitive key on a computer. In bone, it is NFATc1 that seems particularly important.
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