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Controlling bone formation to prevent osteoporosis

Date:
November 7, 2010
Source:
Journal of Clinical Investigation
Summary:
Recent data have suggested that the imbalance between bone formation and bone destruction that causes osteoporosis is a result of a decrease in formation of bone forming osteoblast cells from mesenchymal cells upon aging. New research in mice provides insight into this decrease and might provide new avenues of research for those developing approaches to treat age-related osteoporosis.

Recent data have suggested that the imbalance between bone formation and bone destruction that causes osteoporosis is a result of a decrease in formation of bone forming osteoblast cells from mesenchymal cells upon aging. New research in mice provides insight into this decrease and might provide new avenues of research for those developing approaches to treat age-related osteoporosis.

Aging disrupts the balance between bone formation and bone destruction, resulting in osteoporosis, which is characterized by reduced bone mass and increased risk of fracture. Recent data have suggested that this imbalance is a result of a decrease in formation of bone forming osteoblast cells from mesenchymal cells upon aging. Instead, these cells form more fat cells. Insight into this age-related switch in cell type generation has now been provided by a team of researchers, led by Hiroshi Takayanagi, at Tokyo Medical and Dental University, Japan, working in mice.

The data generated might provide new avenues of research for those developing approaches to treat age-related osteoporosis.

In the study, the gene regulatory protein Maf was found to promote mesenchymal cell generation of osteoblasts and suppress their generation of fat cells. Consistent with this, mice lacking Maf showed delayed bone formation. Furthermore, Maf levels were found to decrease in mouse mesenchymal cells upon aging and to be reduced by increased oxidative stress, something that occurs upon aging. Both the authors and, in an accompanying commentary, Laurie McCauley, at University of Michigan, Ann Arbor, believe these data could lead to new approaches to treat age-related osteoporosis.


Story Source:

The above story is based on materials provided by Journal of Clinical Investigation. Note: Materials may be edited for content and length.


Journal Reference:

  1. Keizo Nishikawa, Tomoki Nakashima, Shu Takeda, Masashi Isogai, Michito Hamada, Ayako Kimura, Tatsuhiko Kodama, Akira Yamaguchi, Michael J. Owen, Satoru Takahashi, Hiroshi Takayanagi. Maf promotes osteoblast differentiation in mice by mediating the age-related switch in mesenchymal cell differentiation. Journal of Clinical Investigation, 2010; DOI: 10.1172/JCI42528

Cite This Page:

Journal of Clinical Investigation. "Controlling bone formation to prevent osteoporosis." ScienceDaily. ScienceDaily, 7 November 2010. <www.sciencedaily.com/releases/2010/09/100927122215.htm>.
Journal of Clinical Investigation. (2010, November 7). Controlling bone formation to prevent osteoporosis. ScienceDaily. Retrieved July 31, 2014 from www.sciencedaily.com/releases/2010/09/100927122215.htm
Journal of Clinical Investigation. "Controlling bone formation to prevent osteoporosis." ScienceDaily. www.sciencedaily.com/releases/2010/09/100927122215.htm (accessed July 31, 2014).

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