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dc.contributor.authorFonseca, Tatiana L.
dc.contributor.authorTeixeira, Marilia B. C. G.
dc.contributor.authorRodrigues-Miranda, Manuela
dc.contributor.authorSilva, Marcos V.
dc.contributor.authorMartins, Gisele M.
dc.contributor.authorCosta, Cristiane C.
dc.contributor.authorArita, Danielle Y. [UNIFESP]
dc.contributor.authorPerez, Juliana D. [UNIFESP]
dc.contributor.authorCasarini, Dulce E. [UNIFESP]
dc.contributor.authorBrum, Patricia C.
dc.contributor.authorGouveia, Cecilia H. A.
dc.identifier.citationAmerican Journal of Physiology-endocrinology and Metabolism. Bethesda: Amer Physiological Soc, v. 307, n. 4, p. E408-E418, 2014.
dc.description.abstractTo 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.en
dc.description.sponsorshipFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.description.sponsorshipCoordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
dc.publisherAmer Physiological Soc
dc.relation.ispartofAmerican Journal of Physiology-endocrinology and Metabolism
dc.rightsAcesso aberto
dc.subjectthyroid hormoneen
dc.subjectsympathetic nervous systemen
dc.titleThyroid hormone interacts with the sympathetic nervous system to modulate bone mass and structure in young adult miceen
dc.contributor.institutionUniversidade de São Paulo (USP)
dc.contributor.institutionUniversidade Federal de São Paulo (UNIFESP)
dc.description.affiliationUniv São Paulo, Inst Biomed Sci, Dept Anat, BR-05508900 São Paulo, Brazil
dc.description.affiliationUniversidade Federal de São Paulo, Sch Med, Dept Internal Med, Div Renal, São Paulo, Brazil
dc.description.affiliationUniv São Paulo, Sch Phys Educ & Sport, BR-05508900 São Paulo, Brazil
dc.description.affiliationUnifespUniversidade Federal de São Paulo, Sch Med, Dept Internal Med, Div Renal, São Paulo, Brazil
dc.description.sponsorshipIDFAPESP: 2010/06409-0
dc.description.sponsorshipIDFAPESP: 2013/02247-3
dc.description.sponsorshipIDFAPESP: 05/59557-8
dc.description.sponsorshipIDFAPESP: 10/50068-2
dc.description.sponsorshipIDFAPESP: 2012/11858-3
dc.description.sponsorshipIDFAPESP: 10/04911-0
dc.description.sponsorshipIDFAPESP: 09/52485-2
dc.description.sourceWeb of Science

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