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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Thyroid hormone interacts with the sympathetic nervous system to modulate bone mass and structure in young adult mice

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Author(s):
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Fonseca, Tatiana L. [1] ; Teixeira, Marilia B. C. G. [1] ; Rodrigues-Miranda, Manuela [1] ; Silva, Marcos V. [1] ; Martins, Gisele M. [1] ; Costa, Cristiane C. [1] ; Arita, Danielle Y. [2] ; Perez, Juliana D. [2] ; Casarini, Dulce E. [2] ; Brum, Patricia C. [3] ; Gouveia, Cecilia H. A. [1]
Total Authors: 11
Affiliation:
[1] Univ Sao Paulo, Inst Biomed Sci, Dept Anat, BR-05508900 Sao Paulo - Brazil
[2] Univ Fed Sao Paulo, Sch Med, Dept Internal Med, Div Renal, Sao Paulo - Brazil
[3] Univ Sao Paulo, Sch Phys Educ & Sport, BR-05508900 Sao Paulo - Brazil
Total Affiliations: 3
Document type: Journal article
Source: AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM; v. 307, n. 4, p. E408-E418, AUG 15 2014.
Web of Science Citations: 7
Abstract

To investigate whether thyroid hormone (TH) interacts with the sympathetic nervous system (SNS) to modulate bone mass and structure, we studied the effects of daily T-3 treatment in a supraphysiological dose for 12 wk on the bone of young adult mice with chronic sympathetic hyperactivity owing to double-gene disruption of adrenoceptors that negatively regulate norepinephrine release, alpha(2A)-AR, and alpha(2C)-AR (alpha(2A/2C)-AR(-/-) mice). As expected, T3 treatment caused a generalized decrease in the areal bone mineral density (aBMD) of WT mice (determined by DEXA), followed by deleterious effects on the trabecular and cortical bone microstructural parameters (determined by mu CT) of the femur and vertebra and on the biomechanical properties (maximum load, ultimate load, and stiffness) of the femur. Surprisingly, alpha(2A/2C)-AR(-/-) mice were resistant to most of these T-3-induced negative effects. Interestingly, the mRNA expression of osteoprotegerin, a protein that limits osteoclast activity, was upregulated and downregulated by T-3 in the bone of alpha(2A/2C)-AR(-/-) and WT mice, respectively. beta(1)-AR mRNA expression and IGF-I serum levels, which exert bone anabolic effects, were increased by T-3 treatment only in alpha(2A/2C)-AR(-/-) mice. As expected, T-3 inhibited the cell growth of calvaria-derived osteoblasts isolated from WT mice, but this effect was abolished or reverted in cells isolated from KO mice. Collectively, these findings support the hypothesis of a TH-SNS interaction to control bone mass and structure of young adult mice and suggests that this interaction may involve alpha(2)-AR signaling. Finally, the present findings offer new insights into the mechanisms through which TH regulates bone mass, structure, and physiology. (AU)

FAPESP's process: 10/04911-0 - Evaluation of the effect of thyroid hormone on bone structure and physiology of mice with gene inactivation of the alpha 2A adrenoceptor
Grantee:Gisele Miyamura Martins
Support Opportunities: Scholarships in Brazil - Master
FAPESP's process: 13/02247-3 - Evaluation of the interaction between thyroid hormone and the sympathetic nervous system, via alpha 2 adrenoceptors, on the regulation of bone growth and maturation
Grantee:Cecilia Helena de Azevedo Gouveia
Support Opportunities: Regular Research Grants
FAPESP's process: 12/11858-3 - Evaluation of the interaction of thyroid hormone with the sympathetic nervous system, via alpha-2 adrenergic receptors, in the regulation of bone growth and maturation
Grantee:Marcos Vinicius da Silva
Support Opportunities: Scholarships in Brazil - Doctorate
FAPESP's process: 10/06409-0 - Evaluation of the effect of thyroid hormone on bone structure and physiology of mice with gene inactivation of alpha 2A and alpha 2C adrenoceptors
Grantee:Cecilia Helena de Azevedo Gouveia
Support Opportunities: Regular Research Grants