
@Article{biocell.2023.029644,
AUTHOR = {DANIELLA M. ADAMS, KALIE F. BECKERS, JULIET P. FLANAGAN, VIVIANE C. L. GOMES, CHIN-CHI LIU, JENNY L. SONES},
TITLE = {Reversal of maternal obesity attenuates hypoxia and improves placental development in the preeclamptic-like BPH/5 mouse model},
JOURNAL = {BIOCELL},
VOLUME = {47},
YEAR = {2023},
NUMBER = {9},
PAGES = {2051--2058},
URL = {http://www.techscience.com/biocell/v47n9/54293},
ISSN = {1667-5746},
ABSTRACT = { <b>Background:</b> Women with obesity have higher risk of adverse pregnancy outcomes, including preeclampsia (PE). Late-gestational hypertension, aberrant fetoplacental development, and fetal growth restriction (FGR), hallmarks of PE, are observed spontaneously in BPH/5 mice. Similar to obese preeclamptic women, BPH/5 mice have higher visceral white adipose tissue (WAT) and circulating leptin. We hypothesized that attenuation of maternal obesity and serum leptin in pregnant BPH/5 mice will improve fetoplacental development by decreasing hypoxia markers and leptin expression at the maternal-fetal interface. <b>Methods:</b> To test this hypothesis, BPH/5 mice were fed <i>ad libitum</i> (lib) and pair-fed (PF) to C57 ad lib controls beginning at embryonic day (e) 0.5. Hypoxia-related genes, hypoxia inducible factor (Hif) 1α, stem cell factor (Scf), heme oxygenase-1 (Ho-1), leptin (Lep), and leptin receptor (LepR) were assessed in e7.5 implantation sites. <b>Results:</b> BPH/5 ad lib had 1.5 to 2-fold increase in <i>Hif1α</i>, <i>Scf</i>, and <i>Ho-1</i> mRNA and a greater than 3-fold increase in leptin mRNA <i>vs</i>. C57 that was attenuated with PF. Exogenous leptin promoted Hif1α and Ho-1 mRNA expression in e7.5 decidua <i>in vitro</i>. While hypoxic conditions <i>in vitro</i> did not change decidual leptin mRNA. Furthermore, BPH/5 PF mice demonstrated improved fetal and placental outcomes later in gestation, with greater placental vascular area by e18.5 and attenuation of FGR. <b>Conclusion:</b> In conclusion, pair-feeding BPH/5 mice beginning at conception may improve placental vasculature formation via decreased leptin and hypoxia-associated markers in this model. Future investigations are needed to better determine the effect of hypoxia and leptin on pregnancy outcomes in obese pregnant women.},
DOI = {10.32604/biocell.2023.029644}
}



