Mechanisms leading to increased risk of preterm birth in growth-restricted guinea pig pregnancies

Hannah K. Palliser, Meredith A. Kelleher, Toni N. Welsh, Tamas Zakar, Jonathan J. Hirst

Research output: Contribution to journalArticlepeer-review

5 Scopus citations

Abstract

Intrauterine growth restriction (IUGR) is a risk factor for preterm labor; however, the mechanisms of the relationship remain unknown. Prostaglandin (PG), key stimulants of labor, availability is regulated by the synthetic enzymes, prostaglandin endoperoxidases 1 and 2 (PTGS1 and 2), and the metabolizing enzyme, 15-hydroxyprostaglandin dehydrogenase (HPGD). We hypothesized that IUGR increases susceptibility to preterm labor due to the changing balance of synthetic and metabolizing enzymes and hence greater PG availability. We have tested this hypothesis using a surgically induced IUGR model in guinea pigs, which results in significantly shorter gestation. Myometrium, amnion, chorion, and placentas were collected from sham operated or IUGR pregnancies, and PTGS1 and HPGD protein expression were quantified throughout late gestation (>62 days) and labor. The PTGS1 expression was significantly upregulated in the myometrium of IUGR animals, and chorionic HPGD expression was markedly decreased (P <.01 and P <.001, respectively). These findings suggest a shift in the balance of PG production over metabolism in IUGR pregnancies leads to a greater susceptibility to preterm birth.

Original languageEnglish (US)
Pages (from-to)269-276
Number of pages8
JournalReproductive Sciences
Volume21
Issue number2
DOIs
StatePublished - Feb 2014
Externally publishedYes

Keywords

  • 15-hydroxyprostaglandin dehydrogenase
  • growth restriction
  • myometrium
  • preterm labor
  • prostaglandins

ASJC Scopus subject areas

  • Obstetrics and Gynecology

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