Human chorionic gonadotropin-dependent regulation of 17β- hydroxysteroid dehydrogenase type 4 in preovulatory follicles and its potential role in follicular luteinization Academic Article uri icon

Overview

MeSH Major

  • 17-Hydroxysteroid Dehydrogenases
  • Chorionic Gonadotropin
  • Follicular Phase
  • Luteinization
  • Ovarian Follicle

abstract

  • 17Beta-hydroxysteroid dehydrogenase type 4 (17betaHSD4) has a unique multidomain structure, with one domain involved in 17beta-estradiol inactivation. The objective of the study was to investigate the regulation of 17betaHSD4 during human chorionic gonadotropin (hCG)-induced ovulation/luteinization. The equine 17betaHSD4 cDNA was cloned and was shown to encode a 735-amino acid protein that is highly conserved (81-87% identity) compared with other mammalian orthologs. RT-PCR/Southern blot analyses were performed to study the regulation of 17betaHSD4 transcripts in equine preovulatory follicles isolated between 0-39 h after hCG treatment. Results showed the presence of basal 17betaHSD4 mRNA expression before hCG treatment, but an increase was observed in follicles obtained 24 h after hCG (P < 0.05). Analyses of isolated preparations of granulosa and theca interna cells identified basal mRNA expression in both layers, but granulosa cells appeared as the predominant site of follicular 17betaHSD4 mRNA induction. A specific polyclonal antibody was raised against a fragment of the equine protein and used to study regulation of the 17betaHSD4 protein. Immunoblots showed an increase in full-length 17betaHSD4 protein in follicles 24 h after hCG (P < 0.05), in keeping with mRNA results. Immunohistochemical data confirmed the induction of the enzyme in follicular cells after hCG treatment. Collectively, these results demonstrate that the gonadotropin-dependent induction of follicular luteinization is accompanied by an increase in 17betaHSD4 expression. Considering the estrogen-inactivating function of 17betaHSD4, its regulated expression in luteinizing preovulatory follicles appears as a potential complementary mechanism to reduce circulating levels of 17beta-estradiol after the LH surge.

publication date

  • April 2004

Research

keywords

  • Academic Article

Identity

Language

  • eng

Digital Object Identifier (DOI)

  • 10.1210/en.2003-1715

PubMed ID

  • 14726434

Additional Document Info

start page

  • 1906

end page

  • 15

volume

  • 145

number

  • 4