Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

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Sims, N.A. et al.

Bone homeostasis in growth hormone receptor-null mice is restored by IGF-I but independent of Stat5.

Growth hormone (GH) regulates both bone growth and remodeling, but it is unclear whether these actions are mediated directly by the GH receptor ( GHR) and/or IGF-I signaling. The actions of GH are transduced by the Jak/ Stat signaling pathway via Stat5, which is thought to regulate IGF-I expression. To determine the respective roles of GHR and IGF-I in bone growth and remodeling, we examined bones of wild-type, GHR knockout ( GHR(-/-)), Stat5ab(-/-), and GHR(-/-) mice treated with IGF-I. Reduced bone growth in GHR(-/-) mice, due to a premature reduction in chondrocyte proliferation and cortical bone growth, was detected after 2 weeks of age. Additionally, although trabecular bone volume was unchanged, bone turnover was significantly reduced in GHR(-/-) mice, indicating GH involvement in the high bone-turnover level during growth. IGF-I treatment almost completely rescued all effects of the GHR(-/-) on both bone growth and remodeling, supporting a direct effect of IGF-I on both osteoblasts and chondrocytes. Whereas bone length was reduced in Stat5ab(-/-) mice, there was no reduction in trabecular bone remodeling or growth-plate width as observed in GHR(-/-) mice, indicating that the effects of GH in bone may not involve Stat5 activation.[1]

References

Bone homeostasis in growth hormone receptor-null mice is restored by IGF-I but independent of Stat5. Sims, N.A., Clément-Lacroix, P., Da Ponte, F., Bouali, Y., Binart, N., Moriggl, R., Goffin, V., Coschigano, K., Gaillard-Kelly, M., Kopchick, J., Baron, R., Kelly, P.A. J. Clin. Invest. (2000) [Pubmed]

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