PUBLICATION

Relaxin-3 and RXFP3 expression, and steroidogenic actions in the ovary of teleost fish

Authors
Wilson, B.C., Burnett, D., Rappaport, R., Parry, L.J., and Fletcher, E.K.
ID
ZDB-PUB-121030-1
Date
2009
Source
Comparative biochemistry and physiology. Part A, Molecular & integrative physiology   153(1): 69-74 (Journal)
Registered Authors
Keywords
follicle, GPCR135, killifish, ovary, relaxin, steroidogenesis, zebrafish
MeSH Terms
  • Animals
  • Estradiol/metabolism
  • Female
  • Fundulidae/metabolism*
  • Gene Expression Regulation
  • Humans
  • Male
  • Ovary/cytology
  • Ovary/metabolism*
  • Receptors, Peptide/genetics
  • Receptors, Peptide/metabolism*
  • Relaxin/genetics
  • Relaxin/metabolism*
  • Reverse Transcriptase Polymerase Chain Reaction
  • Steroids/metabolism*
  • Testis/metabolism
  • Zebrafish/metabolism*
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/metabolism*
PubMed
18852059 Full text @ Comp. Biochem. Physiol. A Mol. Integr. Physiol.
Abstract

Relaxins are peptides similar in secondary structure to insulins. In teleost genomes, five or six relaxin genes have been identified. Two relaxins group closely with mammalian relaxin-3 on phylogenetic analysis and are named relaxin-3a and b. We refer to the remainder as relaxins c to f. Ovarian expression of relaxin-3a, d and f genes, and the relaxin-3 receptor gene Rxfp3, was studied in Danio rerio using RT-PCR. Immunohistochemistry was used to determine the distribution of relaxin-3 peptides and RXFP3 in the ovary of Fundulus heteroclitus (killifish). Thirdly, enzyme immunoassays and ovarian follicular culture were used to determine the effect of treatment with human recombinant relaxin-3 on the production of 17β-estradiol and 17 alpha, 20 beta-dihydroxy-4-pregnen-3-one in killifish ovarian follicles. Relaxin-3a, d, f, and Rxfp3 genes were expressed regardless of sex or reproductive condition. Relaxin-3 immunostaining was present in mid to late follicular stages within cortical alveoli of the oocyte cytopasm, whereas receptor staining was localized to follicular cells. Treatment with relaxin-3 enhanced 17β-estradiol production in early and late maturing follicles, but did not have an effect in vitellogenic follicles. Relaxin-3 appeared to suppress the release of MIS production. This suggests that relaxin peptides may be involved with estradiol-dependant events in follicular development.

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