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Research Article Free access | 10.1172/JCI119729

Regulation of the gp80 and gp130 subunits of the IL-6 receptor by sex steroids in the murine bone marrow.

S C Lin, T Yamate, Y Taguchi, V Z Borba, G Girasole, C A O'Brien, T Bellido, E Abe, and S C Manolagas

Division of Endocrinology, University of Arkansas for Medical Sciences Center for Osteoporosis and Metabolic Bone Diseases, Little Rock, AR 77205, USA.

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Division of Endocrinology, University of Arkansas for Medical Sciences Center for Osteoporosis and Metabolic Bone Diseases, Little Rock, AR 77205, USA.

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Division of Endocrinology, University of Arkansas for Medical Sciences Center for Osteoporosis and Metabolic Bone Diseases, Little Rock, AR 77205, USA.

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Division of Endocrinology, University of Arkansas for Medical Sciences Center for Osteoporosis and Metabolic Bone Diseases, Little Rock, AR 77205, USA.

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Division of Endocrinology, University of Arkansas for Medical Sciences Center for Osteoporosis and Metabolic Bone Diseases, Little Rock, AR 77205, USA.

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Division of Endocrinology, University of Arkansas for Medical Sciences Center for Osteoporosis and Metabolic Bone Diseases, Little Rock, AR 77205, USA.

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Division of Endocrinology, University of Arkansas for Medical Sciences Center for Osteoporosis and Metabolic Bone Diseases, Little Rock, AR 77205, USA.

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Division of Endocrinology, University of Arkansas for Medical Sciences Center for Osteoporosis and Metabolic Bone Diseases, Little Rock, AR 77205, USA.

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Division of Endocrinology, University of Arkansas for Medical Sciences Center for Osteoporosis and Metabolic Bone Diseases, Little Rock, AR 77205, USA.

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Published October 15, 1997 - More info

Published in Volume 100, Issue 8 on October 15, 1997
J Clin Invest. 1997;100(8):1980–1990. https://doi.org/10.1172/JCI119729.
© 1997 The American Society for Clinical Investigation
Published October 15, 1997 - Version history
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Abstract

Both estrogen and androgen exert their antiosteoporotic effects, at least in part, by inhibiting IL-6 production, thereby suppressing osteoclastogenesis. Several observations, however, suggest that besides increased IL-6 production, sensitivity of the osteoclastogenic process to this cytokine is altered after ovariectomy. Based on this and evidence that the ligand-binding subunit of the IL-6 receptor (gp80) is a limiting factor for the actions of IL-6 on bone, we hypothesized that sex steroids regulate expression of the IL-6 receptor as well. We report that 17beta-estradiol or dihydrotestosterone in vitro decreased the abundance of the gp80 mRNA as well as the mRNA of the signal-transducing subunit of the IL-6 receptor (gp130) in cells of the bone marrow stromal/osteoblastic lineage, and also decreased gp130 protein levels. These effects did not require new protein synthesis. In contrast to sex steroids, parathyroid hormone stimulated gp130 expression; this effect was opposed by sex steroids. Consistent with these findings, ovariectomy in mice caused an increase in expression of gp80, gp130, and IL-6 mRNAs in ex vivo bone marrow cell cultures as determined by quantitative reverse transcription (RT)-PCR, and confirmed on an individual cell basis using in situ RT-PCR. The demonstration of increased expression of the IL-6 receptor after loss of sex steroids provides an explanation for why IL-6 is important for skeletal homeostasis in the sex steroid-deficient, but not replete, state.

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