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Gene regulatory protein could hold key to preventing osteoporosis
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Investigators in Japan may have identified at least part of the age-related switch in cell type generation that leads to osteoporosis in an aging population.
The study, recently published in The Journal of Clinical Investigation, found that the gene regulatory protein Maf plays a large part in the late development of osteoporosis on the molecular level.
“This study establishes the crucial role of the Maf-mediated transcriptional program in the physiological and age-related regulation of mesenchymal cell lineage, which may facilitate the development of new therapeutic strategies against bone and metabolic disease,” the authors wrote in their study.
The importance of Maf
With age, cells begin to favor differentiation into adipocytes, resulting in an increased number of adiopocytes and a decreased number of osteoblasts. This causes osteoporosis.
The investigators, led by Hiroshi Takayanagi, MD, PhD, found that with age, the expression of Maf in mouse mesenchymal cells begins to decrease. The Maf in those mesenchymal cells regulates bifurcation into osteoblasts and adipocytes. Without Maf, osteoblast production decreases and the generation of fat cells increases.
Consistent with the study’s findings, investigators noted that mice lacking in Maf showed delayed bone formation and the increased presence of fatty marrow associated with bone loss. Furthermore, Maf levels were found to decrease in mouse mesenchymal cells upon aging – and to be reduced by increased oxidative stress, which occurs with age.
“Haploinsufficiency of Maf results in enhanced adipogenesis and decreased osteogenesis in vivo, which was obvious at an advanced age, suggesting that the decreasing level of Maf with age contributes to the age-related switch in mesenchymal cell differentiation into adipocytes rather than osteoblasts,” the authors wrote.
Reference:
Nihikawa K, Nakashima T, Takeda S, et al.Maf promotes osteoblast differentiation in mice by mediating the age-related switch in mesenchymal cell differentiation. J Clin Invest. Published online. doi:10.1172/JCI42528.
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