It activates a gene critical for the body's tissues to heal and regenerate, says Robert Costa, professor of biochemistry and molecular genetics at the University of Illinois at Chicago and a member of the UIC Cancer Center.
That discovery could help explain why we age.
"Growth hormone levels decline as we grow older; as a result, the Foxm1b gene stops working and our bodies are less capable of repairing damage," Costa said.
In a paper published in the December issue of Hepatology, Costa and his colleagues report the results of studies on liver regeneration in aged (12-month-old) and young (2-month-old) mice -- a model system for studying the molecular mechanisms the body enlists to restore tissue damaged by injury or age. The liver is the only organ in the body capable of completely regenerating from mature cells.
The scientists focused on the Foxm1b gene, which is involved in the entire life cycle of the mammalian cell -- its proliferation, maturation and death. The gene's activity is elevated in dividing cells in young mammals but diminishes in old age.
In previous studies, the researchers inserted the human Foxm1b gene in aged mice whose livers had been partially removed (the two species have virtually identical forms of the gene). The experiments showed that the gene restored levels of Foxm1b proteins and induced the animals' livers to grow back at a rate typical of young mice. Further research detailed how the gene directs the busy molecular traffic inside cells to make them divide and multiply.
In the present study, the scientists tested the effects of human growth hormone because of its purported role in stimulating cell proliferation. Growth hormone, a substance secreted by the pituitary gland in the brain, is responsible for growth in children and young adults, but its levels decline
Contact: Sharon Butler
University of Illinois at Chicago