BoneKEy Reports | BoneKEy Watch
TSH acts directly on osteoblasts to increase bone production
DOI:10.1038/bonekey.2012.7
Previous studies have shown that thyroid stimulating hormone (TSH) prevents bone loss and stimulates bone formation when administered in vivo. As well as inhibiting osteoclast activity, TSH might also stimulate bone formation by targeting osteoblast TSH receptors (TSHR).
Baliram et al. investigated this possibility using TSHR-positive embryonic stem (ES) cells in an experimental culture system. They first showed that ES cells can differentiate into mature, mineralising osteoblasts; this could, suggest the authors, explain the anabolic action of TSH in vivo.
Further experiments demonstrated that TSH was able to functionally stimulate osteoblast differentiation by activating the noncanonical Wnt pathway that is downstream of protein kinase Cδ. Wnt signalling may increase bone mass directly and indirectly. It boosts osteoblastogenesis and bone formation, but also stimulates osteoblasts to produce osteoprotegerin (OPG), which then inhibits RANK-L-induced osteoclastogenesis and bone resorption.
The authors propose that TSH acts via a short feedback loop in which TSH increases the expression of WNT5a, which encourages osteoblastogenesis and also increases OPG production, which then reduces osteoclastic resorption with an additional positive impact on bone mass.
Editor's comment: Bone is a target organ for a number of pituitary hormones. Here the direct influence of TSH on osteoblast differentiation is shown using ES cells in vitro. Results of further in vitro tests suggest that TSH uncouples bone formation from bone resorption by its action on osteoblasts within the skeleton.
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