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Doctoral Thesis
DOI
10.11606/T.42.2014.tde-12082014-194142
Document
Author
Full name
Cristiane Cabral Costa
Institute/School/College
Knowledge Area
Date of Defense
Published
São Paulo, 2014
Supervisor
Committee
Ferreira, Cecilia Helena de Azevedo Gouveia (President)
Bueno, Maria Rita dos Santos e Passos
Castro, Marise Lazaretti
Chavez, Victor Elias Arana
Pereira, Rosa Maria Rodrigues
Title in Portuguese
Efeito do hormônio tireoideano e do seu antagonista NH3 na diferenciação osteoblástica de células mesenquimais periósticas humanas portadoras de mutação no FGFR2 determinante da Síndrome de Apert.
Keywords in Portuguese
Antagonista do T3
Diferenciação osteoblástica
Hormônio tireoideano
Mutação P253R
NH3
Síndrome de Apert
Abstract in Portuguese
Evidências sugerem interação entre o hormônio tireoideano (T3) e os fatores de crescimento fibroblásticos (FGF) no desenvolvimento esquelético. Para estudarmos essa interação, avaliamos o efeito do T3 e do seu antagonista NH3 em células mesenquimais periósticas humanas de pacientes normais e portadores da Síndrome de Apert (SA), que é caracterizada por craniossinostose e causada por mutações no receptor de FGF tipo 2 (FGFR2). Nas células SA, o T3 aumentou o número de células e o NH3 bloqueou esse efeito do T3. O T3 e/ou NH3 aumentaram a atividade da fosfatase alcalina durante a diferenciação osteoblástica das células normais, mas não das mutadas. O T3 aumentou a diferenciação osteoblástica e o NH3 bloqueou esse efeito do T3 em células normais. Nas células mutadas, o NH3 limitou a diferenciação osteoblástica, enquanto o T3 não teve efeito. Concluímos que as células mesenquimais periósticas humanas normais e SA são responsivas ao T3 e NH3, e que o T3 e FGF podem atuar através de vias de sinalização comuns na regulação da diferenciação osteoblástica.
Title in English
Effect of thyroid hormone and its antagonist NH3 in osteoblastic differentiation of human periosteal mesenchymal cells with mutation in FGFR2 that cause Apert Syndrome.
Keywords in English
Apert Syndrome
NH3
Osteoblastic differentiation
P253R mutation
T3 antagonist
Thyroid hormone
Abstract in English
Evidence suggests that there is an interaction between the thyroid hormone (T3) and fibroblast growth factors (FGFs) in the skeletal development. To study this interaction, we evaluated the effect of T3 and its antagonist, NH3, in human periosteal mesenchymal cells from normal and Apert Syndrome (AS) patients, which is characterized by craniosynostosis and is caused by mutations in FGF receptor type 2 (FGFR2). In AS cells, the T3 increased the number of cells and NH3 blocked this effect of T3. T3 and/or NH3 increased the alkaline phosphatase activity in osteoblast differentiation of normal cells, but not in the mutated cells. T3 increased osteoblast differentiation and NH3 blocked this effect of T3 on normal cells. In the mutated cells, NH3 limited osteoblast differentiation while T3 had no effect. We concluded that normal and AS human periosteal mesenchymal cells are responsive to T3 and NH3, and T3 and FGF may act through common signaling pathways in the regulation of osteoblastic differentiation.
 
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Publishing Date
2014-08-14
 
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