With aging comes bone loss – in both genders and across all ethnic backgrounds. To search for factors that may link aging and maintenance of bone mass, Florent Elefteriou, Ph.D., director of the Vanderbilt Center for Bone Biology, and colleagues examined the role of sirtuin1 (SirT1), a gene associated with cell survival and longevity.
They showed that SirT1 expression is reduced in normal aging bones in mice. Deletion of the SirT1 gene specifically in osteoblasts (bone-forming cells) or osteoclasts (bone-removing cells) in mice resulted in reduced bone mass, caused by reduced bone formation or increased bone resorption (removal). Lack of SirT1 in bone cells reduced osteoblast maturation, promoted the production of new osteoclasts, and activated NF-kB signaling in both cell types. Pharmacologic inhibition of NF-kB blocked the effects of missing SirT1.
The findings, published in the Journal of Bone and Mineral Research, suggest that SirT1 participates in the normal regulation of bone remodeling through control of NF-kB activity and that it may be involved in bone loss associated with aging.
This research was supported by the American Federation for Aging Research, the Vanderbilt Department of Medicine and the Vanderbilt Orthopaedic Institute.
