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Thyroid Hormone Stimulates the Proliferation of Sertoli Cells and Single Type A Spermatogonia in Adult Zebrafish (Danio rerio) Testis
  • Universidade Federal de Minas Gerais (UFMG)
  • Univ Utrecht
  • Universidade Estadual Paulista (UNESP)
  • Fundação de Amparo à Pesquisa do Estado de Minas Gerais (FAPEMIG)
  • European Union LIFE CYCLE project
  • Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
  • Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
Sponsorship Process Number: 
European Union LIFE CYCLE projectFP7/222719
Thyroid hormones participate in regulating growth and homeostatic processes in vertebrates, including development and adult functioning of the reproductive system. Here we report a new stimulatory role of thyroid hormone on the proliferation of Sertoli cells (SCs) and single, type A undifferentiated spermatogonia (A(und)) in adult zebrafish testes. A role for T-3 in zebrafish testis is suggested by in situ hybridization studies, which localized thyroid receptor alpha (thr alpha) in SCs and the beta (thr beta) mRNA in Sertoli and Leydig cells. Using a primary zebrafish testis tissue culture system, the effect of T-3 on steroid release, spermatogenesis, and the expression of selected genes was evaluated. Basal steroid release and Leydig cell gene expression did not change in response to T-3. However, in the presence of FSH, T-3 potentiated gonadotropin-stimulated androgen release as well as androgen receptor (ar) and 17 alpha-hydroxylase/17,20 lyase (cyp17a1) gene expression. Moreover, T-3 alone stimulated the proliferation of both SCs and A(und), potentially resulting in newly formed spermatogonial cysts. Additional tissue culture studies demonstrated that Igf3, a new, gonad-specific member of the IGF family, mediated the stimulatory effect of T-3 on the proliferation of A(und) and SCs. Finally, T-3 induced changes in connexin 43 mRNA levels in the testis, a known T-3-responsive gene. Taken together, our studies suggest that T-3 expands the population of SCs and A(und) involving Igf signaling and potentiates gonadotropin-stimulated testicular androgen production as well as androgen sensitivity.
Issue Date: 
Endocrinology. Chevy Chase: Endocrine Soc, v. 154, n. 11, p. 4365-4376, 2013.
Time Duration: 
Endocrine Soc
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Appears in Collections:Artigos, TCCs, Teses e Dissertações da Unesp

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