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Connecting Bone and Fat: the Potential Role for Sclerostin

  • Molecular Biology of Skeletal Development (T Bellido, Section Editor)
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Abstract

Purpose of Review

Sclerostin (SOST), a protein secreted from mature osteocytes in response to mechanical unloading and other stimuli, inhibits the osteogenic Wnt/β-catenin pathway in mesenchymal stem cells (MSCs) impeding their ability to differentiate into mineralizing osteoblasts. This review summarizes the crosstalk between adipose tissue and the bone. It also reviews the origin, regulation, and role of SOST in osteogenesis and brings attention to an emerging role of this protein in the regulation of adipogenesis.

Recent Findings

Bone-derived molecules that drive MSC adipogenesis have not previously been identified, but recent findings suggest that SOST signaling may induce adipogenesis. In vivo SOST acts locally to induce changes in the bone and, in vitro, increases adipogenesis in 3T3-L1 preadipocytes.

Summary

SOST is able to induce adipogenesis in certain preadipocytes, however, bone-specific studies are needed to determine the effect of local SOST concentrations in healthy and disease models on bone marrow adipose tissue.

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Acknowledgements

The authors’ work is supported by MMCRI Start-up funds, a pilot project grant from the NIH/NIGMS (P30GM106391) and the NIH/NIDDK (R24DK092759-01).

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Correspondence to Michaela R. Reagan.

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Heather Fairfield, Clifford J. Rosen, and Michaela R. Reagan each declare no potential conflicts of interest.

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This article does not contain any studies with human or animal subjects performed by any of the authors.

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This article is part of the Topical Collection on Molecular Biology of Skeletal Development

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Fairfield, H., Rosen, C.J. & Reagan, M.R. Connecting Bone and Fat: the Potential Role for Sclerostin. Curr Mol Bio Rep 3, 114–121 (2017). https://doi.org/10.1007/s40610-017-0057-7

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