Evaluation of the interaction of thyroid hormone with the sympathetic nervous system, via beta2 adrenergic receptor, in regulation of the mass and bone metabolism

• Grant number: 15/12554-6
• Support type: Scholarships in Brazil - Master
• Effective date (Start): February 01, 2016
• Effective date (End): January 31, 2018
• Field of knowledge: Biological Sciences - Biology
• Principal Investigator: Cecilia Helena de Azevedo Gouveia
• Grantee: Bianca Neofiti Papi
• Home Institution: Instituto de Ciências Biomédicas (ICB). Universidade de São Paulo (USP). São Paulo , SP, Brazil

Abstract

Thyroid hormone (TH) is essential for bone development, maturation and metabolism. Recently, the sympathetic nervous system (SNS) was identified as a potent regulator of bone remodeling. A series of studies suggests that SNS negatively regulates bone mass, via Beta2 adrenoceptor (Beta2-AR), which is expressed in osteoblasts. Considering that TH interacts with SNS to regulate several physiological processes, and that TH excess and SNS activation result in bone loss, we hypothesized that TH interacts with SNS to regulate bone metabolism and, consequently, bone mass. Recent studies by our group have sustained this hypothesis, since mice with the gene inactivation of Alfa2 adrenoceptors (Alfa2-AR) are resistent to the osteopenia induced by toxic doses of TH. These studies have also demonstrated that Alfa2-ARs mediate SNS actions in the skeleton as well. On the other hand, there is no doubt that Beta2-AR has an important role mediating SNS actions in the skeleton. Furthermore, the TH-SNS interaction in other tissues or organs depends of Beta2-AR signaling. In the present study, we will evaluate the effect of TH on bone structure and physiology of mice with gene inactivation of Beta2-AR, aiming to investigate if the TH-SNS interaction to regulate these parameters also depend on Beta2-AR signaling. (AU)