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Effect of thyroid hormone T3 on Myosin-Va expression in the central nervous system
  • Universidade Federal do Rio de Janeiro (UFRJ)
  • Univ Fed Estado Rio de Janeiro
  • Univ Portsmouth
  • Universidade Estadual Paulista (UNESP)
  • McLaughlin Res Inst
  • Univ Castelo Branco
  • Universidade Federal de Uberlândia (UFU)
  • Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
  • Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
  • Fundação de Amparo à Pesquisa do Estado do Rio de Janeiro (FAPERJ)
  • Programa de Apoio aos Núcleos de Excelência (PRONEX)
  • NIH
Sponsorship Process Number: 
  • CAPES: 542/2006
  • PRONEX: 171.546/2006
  • NIH: R01 GM066901
Thyroid hormones (THs) are essential for brain development, where they regulate gliogenesis, myelination, cell proliferation and protein synthesis. Hypothyroidism severely affects neuronal growth and establishment of synaptic connections. Triiodothyronine (T3), the biologically active form of TH, has a central function in these activities. So, Myosin-Va (Myo-Va), a molecular motor protein involved in vesicle and RNA transport, is a good candidate as a target for T3 regulation. Here, we analyzed Myo-Va expression in euthyroid and hypothyroid adult rat brains and synaptosomes. We observed a reduction of Myo-Va expression in cultured neural cells from newborn hypothyroid rat brain, while immunocytochemical experiments showed a punctate distribution of this protein in the cytoplasm of cells. Particularly, Myo-Va co-localized with microtubules in neurites, especially in their varicosities. Myo-Va immunostaining was stronger in astrocytes and neurons of controls when compared with hypothyroid brains. In addition, supplementation of astrocyte cultures with T3 led to increased expression of Myo-Va in cells from both euthyroid and hypothyroid animals, suggesting that T3 modulates Myo-Va expression in neural cells both in vivo and in vitro. We have further analyzed Myo-Va expression in U373 cells, a human glioblastoma line, and found the same punctate cytoplasmic protein localization. As in normal neural cells, this expression was also increased by T3, suggesting that the modulatory mechanism exerted by T3 over Myo-Va remains active on astrocyte tumor cells. These data, coupled with the observation that Myo-Va is severely affected in hypothyroidism, support the hypothesis that T3 activity regulates neural motor protein expression, taking Myo-Va as a model. As a consequence, reduced T3 activity could supposedly affect axonal transport and synaptic function, and could therefore explain disturbances seen in the hypothyroid brain. (C) 2009 Elsevier B.V. All rights reserved.
Issue Date: 
Brain Research. Amsterdam: Elsevier B.V., v. 1275, p. 1-9, 2009.
Elsevier B.V.
  • Myosin-Va
  • Neuron
  • Astrocyte
  • Astroglioma
  • Hypothyroidism
  • T3
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Appears in Collections:Artigos, TCCs, Teses e Dissertações da Unesp

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