PUBLICATION

Involvement of estradiol-17beta and its membrane receptor, G protein coupled receptor 30 (GPR30) in regulation of oocyte maturation in zebrafish, Danio rario

Authors
Pang, Y., and Thomas, P.
ID
ZDB-PUB-081029-21
Date
2009
Source
General and comparative endocrinology   161(1): 58-61 (Journal)
Registered Authors
Keywords
G protein-coupled receptor 30, GPR30, Oocyte maturation, Aromatase inhibitor, Meiosis arrest
MeSH Terms
  • Androstatrienes/pharmacology
  • Animals
  • Aromatase Inhibitors/pharmacology
  • Cyclopentanes/pharmacology
  • Estradiol/analogs & derivatives
  • Estradiol/metabolism*
  • Estradiol/pharmacology
  • Female
  • Hydroxyprogesterones/pharmacology
  • Oocytes/physiology*
  • Quinolines/pharmacology
  • Receptors, Estradiol/agonists
  • Receptors, Estradiol/physiology*
  • Receptors, G-Protein-Coupled/agonists
  • Receptors, G-Protein-Coupled/physiology*
  • Tamoxifen/pharmacology
  • Zebrafish
  • Zebrafish Proteins/physiology*
PubMed
18952087 Full text @ Gen. Comp. Endocrinol.
Abstract
The orphan G protein coupled receptor, GPR30, has the characteristics of a high affinity, specific estrogen membrane receptor on Atlantic croaker oocytes and mediates estrogen inhibition of oocyte maturation in this perciform fish. In order to determine the broad applicability of these findings to other teleosts, similar experiments were conducted in a cyprinid fish, zebrafish, in the present study. GPR30 mRNA expression was detected in zebrafish oocytes but not in the ovarian follicular cells. Both spontaneous and 17, 20beta-dihyroxy-4-pregnen-3-one (DHP)-induced maturation of follicle-enclosed zebrafish oocytes was significantly decreased when they were incubated with either estradiol-17beta, or the GPR30 agonists, ICI 182 780 and tamoxifen, or with the GPR30 specific agonist G-1. On the other hand spontaneous oocyte maturation increased two-fold when zebrafish ovarian follicles were incubated with an aromatase inhibitor, ATD. Moreover, the stimulatory effects of ATD on germinal vesicle breakdown (GVBD) were partially reversed by co-treatment with 100 nM of E2 or G-1. These results suggest that endogenous estrogens acting through GPR30 are involved in maintaining meiotic arrest of zebrafish oocytes.
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