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Theriogenology2005; 64(6); 1371-1380; doi: 10.1016/j.theriogenology.2005.02.015

Expression of mRNA encoding insulin-like growth factor binding protein-2 (IGFBP-2) during induced and natural regression of equine corpora lutea.

Abstract: The insulin-like growth factors, IGF-I and -II, have been shown to play a key role in luteal function in some species. The IGF binding proteins, IGFBP-2 and -3, have been shown to inhibit binding of IGF-I and -II to bovine luteal cells and decrease progesterone production. We have recently shown that equine follicles have the genetic capacity to produce IGFBP-2, and that levels decrease in healthy preovulatory follicles. In the present study expression of mRNAs encoding IGFBP-2, as well as the rate-limiting steroidogenic enzyme, P450scc, were studied in equine corpora lutea to investigate whether IGFBP-2 might be involved in luteolysis. Corpora lutea were collected from mares in mid-luteal phase (day 10), at early regression (day 14), late regression (day 17), and 12 and 36 h after intramuscular administration of the PGF(2alpha) analogue, cloprostenol (0.5 microg/kg). During early natural regression, and 12 h after administration of cloprostenol on day 10, steady state levels of mRNAs encoding P450scc had decreased significantly compared with day 10 of dioestrus (P < 0.001). Levels of mRNA encoding IGFBP-2 increased significantly between mid-diestrus and early (P < 0.01) and late (P < 0.001) regression, and 36 h after cloprostenol administration (P < 0.001). We conclude that the genetic capacity for increased IGFBP-2 production in the early stages of natural luteolysis in the mare may act to sequester IGF-I in the CL, assisting in inhibition of progesterone production. However the delay in increase in mRNA encoding IGFBP-2 after cloprostenol administration, combined with the sharp fall in expression of P450scc mRNA, suggests that the luteolytic action of a pharmacological dose of cloprostenol may not be mediated via IGFBP-2 in the mare.
Publication Date: 2005-04-25 PubMed ID: 16139613DOI: 10.1016/j.theriogenology.2005.02.015Google Scholar: Lookup
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  • Journal Article
  • Research Support
  • Non-U.S. Gov't

Summary

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This research article investigates the role of insulin-like growth factor binding protein-2 (IGFBP-2) in luteolysis, the degradation of the corpus luteum, in horses. The study finds evidence of increased potential for IGFBP-2 production in the early stages of natural luteolysis, which may assist in inhibiting progesterone production, but doesn’t deem IGFBP-2 to be a mediator in luteolysis triggered by a pharmacological dose.

Understanding the Context

  • The research focuses on the role of insulin-like growth factor binding proteins (IGFBP), specifically IGFBP-2 and its impact on luteal function—the performance of the corpus luteum. Corpus luteum is an endocrine structure that forms in an ovary after an ovum is released from the follicle during ovulation and which secretes progesterone.
  • The insulin-like growth factors (IGF) I and II are known to play an important role in luteal function. However, IGFBP-2 and -3 are capable of inhibiting the binding of IGF and lowering progesterone levels.

Research Methods

  • The researchers collected corpora lutea (plural of corpus luteum) from female horses at different stages of the luteal phase: mid-luteal (day 10), early regression (day 14), and late regression (day 17). Two additional collections were done 12 and 36 hours after injecting the animals with cloprostenol, a synthetic form of the hormone prostaglandin F2α commonly used to induce luteolysis.

Insights and Findings

  • The level of mRNA coding for P450scc, a key enzyme involved in steroidogenesis, decreases significantly during early natural regression and 12 hours after administering cloprostenol.
  • On the other hand, the level of mRNA coding for IGFBP-2 significantly increases between mid-diestrus and during both early and late regression as well as 36 hours after the cloprostenol injection.

Conclusions

  • The researchers deduce that the observed increased capability of producing IGFBP-2 in the early phases of natural luteolysis appears to restrict IGF-I within the corpus luteum, aiding in the inhibition of progesterone production.
  • Despite this, the delay in the spike in IGFBP-2 mRNA following cloprostenol administration, along with the rapid decrease in P450scc mRNA suggests the luteolysis, brought on by this pharmacological intervention, may not involve IGFBP-2.

Cite This Article

APA
Watson ED, Bae SE, Al-Zi'abi MO, Hogg CO, Armstrong DG. (2005). Expression of mRNA encoding insulin-like growth factor binding protein-2 (IGFBP-2) during induced and natural regression of equine corpora lutea. Theriogenology, 64(6), 1371-1380. https://doi.org/10.1016/j.theriogenology.2005.02.015

Publication

ISSN: 0093-691X
NlmUniqueID: 0421510
Country: United States
Language: English
Volume: 64
Issue: 6
Pages: 1371-1380

Researcher Affiliations

Watson, E D
  • Royal (Dick) School of Veterinary Studies, Department of Veterinary Clinical Studies, Veterinary Field Station, University of Edinburgh, Easter Bush, Midlothian, Scotland EH25 9RG, UK. elaine.watson@ed.ac.uk
Bae, S-E
    Al-Zi'abi, M O
      Hogg, C O
        Armstrong, D G

          MeSH Terms

          • Animals
          • Cloprostenol / pharmacology
          • Corpus Luteum / chemistry
          • Female
          • Gene Expression
          • Horses
          • Insulin-Like Growth Factor Binding Protein 2 / genetics
          • Insulin-Like Growth Factor Binding Protein 2 / metabolism
          • Insulin-Like Growth Factor I / genetics
          • Insulin-Like Growth Factor I / physiology
          • Insulin-Like Growth Factor II / genetics
          • Insulin-Like Growth Factor II / physiology
          • Luteolysis / drug effects
          • Luteolysis / metabolism
          • Progesterone / blood
          • RNA, Messenger / analysis

          Citations

          This article has been cited 1 times.
          1. Suvorov A, Waxman DJ. Early programing of uterine tissue by bisphenol A: Critical evaluation of evidence from animal exposure studies. Reprod Toxicol 2015 Nov;57:59-72.