The effect of maternal pravastatin therapy on adverse sensorimotor outcomes of the offspring in a murine model of preeclampsia

Alissa R. Carver, Esther Tamayo, J. Regino Perez-Polo, George R. Saade, Gary D.V. Hankins, Maged M. Costantine

Research output: Contribution to journalArticle

21 Scopus citations

Abstract

Animal and human studies show that in-utero exposure to preeclampsia alters fetal programming and results in long-term adverse cardiovascular outcomes in the offspring. Human epidemiologic data also suggest that offspring born to preeclamptic mothers are also at risk of adverse long term neurodevelopmental outcomes. Pravastatin, a hydrophilic lipid-lowering drug with pleiotropic properties, was found to prevent the altered cardiovascular phenotype of preeclampsia and restore fetal growth in animal models, providing biological plausibility for its use as a preventive agent for preeclampsia. In this study, we used a murine model of preeclampsia based on adenovirus over-expression of the anti-angiogenic factor soluble Fms-like tyrosine kinase 1, and demonstrated that adult offspring born to preeclamptic dams perform poorly on assays testing vestibular function, balance, and coordination, and that prenatal pravastatin treatment prevents impairment of fetal programming.

Original languageEnglish (US)
Pages (from-to)33-40
Number of pages8
JournalInternational Journal of Developmental Neuroscience
Volume33
Issue number1
DOIs
StatePublished - Apr 1 2014

Keywords

  • Fetal programming
  • Neuromotor function
  • Pravastatin
  • Preeclampsia
  • Soluble Fms-like tyrosine kinase 1

ASJC Scopus subject areas

  • Developmental Neuroscience
  • Developmental Biology

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