Bone corticalization requires local SOCS3 activity and is promoted by androgen action via interleukin-6

Dae-Chul Cho, Holly J. Brennan, Rachelle W. Johnson, Ingrid J. Poulton, Jonathan H. Gooi, Brett A. Tonkin, Narelle E. McGregor, Emma C. Walker, David J. Handelsman, T. J. Martin and Natalie A. Sims ()
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Dae-Chul Cho: St. Vincent’s Institute of Medical Research
Holly J. Brennan: St. Vincent’s Institute of Medical Research
Rachelle W. Johnson: St. Vincent’s Institute of Medical Research
Ingrid J. Poulton: St. Vincent’s Institute of Medical Research
Jonathan H. Gooi: University of Melbourne
Brett A. Tonkin: St. Vincent’s Institute of Medical Research
Narelle E. McGregor: St. Vincent’s Institute of Medical Research
Emma C. Walker: St. Vincent’s Institute of Medical Research
David J. Handelsman: University of Sydney
T. J. Martin: St. Vincent’s Institute of Medical Research
Natalie A. Sims: St. Vincent’s Institute of Medical Research

Nature Communications, 2017, vol. 8, issue 1, 1-13

Abstract: Abstract Long bone strength is determined by its outer shell (cortical bone), which forms by coalescence of thin trabeculae at the metaphysis (corticalization), but the factors that control this process are unknown. Here we show that SOCS3-dependent cytokine expression regulates bone corticalization. Young male and female Dmp1Cre.Socs3 f/f mice, in which SOCS3 has been ablated in osteocytes, have high trabecular bone volume and poorly defined metaphyseal cortices. After puberty, male mice recover, but female corticalization is still impaired, leading to a lasting defect in bone strength. The phenotype depends on sex-steroid hormones: dihydrotestosterone treatment of gonadectomized female Dmp1Cre.Socs3 f/f mice restores normal cortical morphology, whereas in males, estradiol treatment, or IL-6 deletion, recapitulates the female phenotype. This suggests that androgen action promotes metaphyseal corticalization, at least in part, via IL-6 signaling.

Date: 2017
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DOI: 10.1038/s41467-017-00920-x

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