Researchers studying the effects of aging on bone deterioration in mice found the gene Maf regulates the creation of cells responsible for bone formation or degradation.
The team, led by Keizo Nishikawa of Tokyo Medical and Dental University in Japan, believe the discovery may provide a molecular basis for preventing or treating age-related osteoporosis.
Bone marrow contains mesenchymal cells, capable of forming a variety of cell types. These include osteoblasts, which promote bone growth, and adipocytes, which lay down marrow fat.
As the body ages, mesenchymal cells are more likely to differentiate into adipocytes, which inhibit bone formation and lay down marrow fat, therefore causing osteoporosis.
This effect is also seen in diabetic patients taking thiazolidinediones, suggesting that treatment to alleviate this process could have benefits for osteoporosis related to age and drug use.
Researchers screened the mouse genome for mRNAs expressed in bone formation, which identified Maf.
In healthy mice, Maf regulates the creation of osteoblasts and adipocytes by cooperating with transcription factor Runx2. It also downregulates Pparg, a gene causes aggregation of marrow fat.
Mice bred to lack functioning Maf genes suffered impaired bone formation and accelerated age-related osteoporosis.
Researchers found that at least some of the age-related decline in Maf expression was due to oxidative stress, known to play a role in disrupting biological systems in aging.
The authors concluded: ‘The modulation of Maf expression appears to hold considerable promise as what we believe to be a novel antiaging therapeutic target in the skeletal system.’