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Researcher to study astronaut bone loss for space biology agency

ght. "This makes their rehabilitation risky, because, like astronauts who have returned to earth, they are predisposed to fractures."

Long's research project will focus on the relationship between three substances: insulin-like growth factor-1 (IGF-1), a chemical produced in bone and other organs that promotes the growth of bone and cartilage; IGF-1 receptor, which resides in bone cells and enables them to respond to IGF-1; and beta-3 integrin, a protein that among other roles promotes the function of IGF-1 receptor.

Long's and Bikle's hypothesis is that during prolonged weightlessness, beta-3 integrin production decreases, which in turn diminishes the function of IGF-1 receptor in bone. Without its receptor, IGF-1 has been shown by researchers to be ineffective. The result is a steep drop in the creation of new bone cells, leading to bone loss.

To investigate the hypothesis, Long will take a two-pronged research approach. In the first part, he will study a model of skeletal loading and unloading in human bone cell culture. In the second part, skeletally unloaded rats will be treated with IGF-1 and reloaded on a regular cycle –?much as astronauts might regularly engage in weight-bearing exercise while in orbit –?in order to stimulate integrin production and enhance or recover IGF-1 receptor function. The IGF-1 will act as a signaling device to allow Long to measure the strength of the interaction between integrins and IGF-1 receptor.

"Understanding this interaction, and the role it plays in how bones respond to mechanical forces, will allow interventions to protect the bones of astronauts," Long says.

"We hope to find that we can manipulate the IGF-1 system to accelerate rehabilitation, not only among astronauts but among a broad range of patients," says Bikle. "We might also learn how to prevent bone loss from taking place."

Long concludes, "I am excited and honored to contribute to our nation's efforts
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Source:University of California - San Francisco


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