PUBLICATION

Involvement of cyclic adenosine 3',5'-monophosphate in the differential regulation of activin betaA and betaB expression by gonadotropin in the zebrafish ovarian follicle cells

Authors
Wang, Y. and Ge, W.
ID
ZDB-PUB-030210-7
Date
2003
Source
Endocrinology   144(2): 491-9 (Journal)
Registered Authors
Keywords
none
MeSH Terms
  • Cells, Cultured
  • Gene Expression/drug effects
  • Gene Expression/physiology
  • Bucladesine/pharmacology
  • Phosphodiesterase Inhibitors/pharmacology
  • Cyclic AMP/metabolism*
  • Amino Acid Sequence
  • Colforsin/pharmacology
  • DNA, Complementary
  • Inhibin-beta Subunits/genetics*
  • Gonadotropins/pharmacology*
  • Cyclic AMP-Dependent Protein Kinases/metabolism
  • 1-Methyl-3-isobutylxanthine/pharmacology
  • Zebrafish
  • Reverse Transcriptase Polymerase Chain Reaction/standards
  • Female
  • Humans
  • Molecular Sequence Data
  • Reproducibility of Results
  • Cloning, Molecular
  • Ovarian Follicle/cytology
  • Ovarian Follicle/physiology*
  • Animals
PubMed
12538609 Full text @ Endocrinology
Abstract
Activin is a dimeric protein consisting of two similar but distinct beta -subunits, betaA and betaB. In our previous studies, both activin A ( betaAbetaA) and activin B (betaBbetaB) have been demonstrated to stimulate oocyte maturation and promote oocyte maturational competence in the zebrafish. Follistatin, a specific activin-binding protein, can block both activin- and gonadotropin-induced final oocyte maturation in vitro, suggesting that activin is likely a downstream mediator of gonadotropin actions in the zebrafish ovary. In the present study, a full-length cDNA encoding zebrafish ovarian activin betaA was cloned and sequenced. The precursor of zebrafish activin betaA consists of 395 amino acids and its mature region exhibits about 78% homology with that of mammals. Using an in vitro primary culture of the ovarian follicle cells and semiquantitative RT-PCR assays, we examined the regulation of activin betaA and betaB expression by human chorionic gonadotropin (hCG ) and its intracellular signal transduction mechanisms. hCG (15 IU/ml) increased the mRNA level of activin betaA-subunit; however, it significantly down-regulated the steady-state expression level of activin betaB in a time- and dose-dependent manner. The differential regulation of the two beta-subunits by hCG could be mimicked by 3- isobutyl-1-methylxanthine, forskolin, and dibutyryl-cAMP, suggesting involvement of the intracellular cAMP pathway. Interestingly, H89 (a specific inhibitor of protein kinase A, PKA) could effectively block hCG - and forskolin-stimulated activin betaA expression at 10 micro M, but it was unable to reverse the inhibitory effects of hCG and forskolin on betaB expression. This suggests that the hCG-stimulated activin betaA expression is dependent on the activation of the cAMP-PKA pathway, whereas the inhibitory effect of hCG on activin betaB expression is likely mediated by PKA-independent pathway(s).
Genes / Markers
Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping