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      Augmented Wnt signaling in a mammalian model of accelerated aging.

      Science (New York, N.Y.)

      Wnt3 Protein, Aging, physiology, Animals, Apoptosis, Bone Density, Bone and Bones, metabolism, Cell Aging, Cell Count, Cell Line, Cell Shape, Glucuronidase, chemistry, genetics, Humans, Mice, Mice, Transgenic, Protein Structure, Tertiary, Signal Transduction, Stem Cells, cytology, Wnt Proteins, antagonists & inhibitors, Wnt1 Protein

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          Abstract

          The contribution of stem and progenitor cell dysfunction and depletion in normal aging remains incompletely understood. We explored this concept in the Klotho mouse model of accelerated aging. Analysis of various tissues and organs from young Klotho mice revealed a decrease in stem cell number and an increase in progenitor cell senescence. Because klotho is a secreted protein, we postulated that klotho might interact with other soluble mediators of stem cells. We found that klotho bound to various Wnt family members. In a cell culture model, the Wnt-klotho interaction resulted in the suppression of Wnt biological activity. Tissues and organs from klotho-deficient animals showed evidence of increased Wnt signaling, and ectopic expression of klotho antagonized the activity of endogenous and exogenous Wnt. Both in vitro and in vivo, continuous Wnt exposure triggered accelerated cellular senescence. Thus, klotho appears to be a secreted Wnt antagonist and Wnt proteins have an unexpected role in mammalian aging.

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          Journal
          10.1126/science.1143578
          17690294

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