Placental mitochondrial dysfunction in pregnancies complicated by asthma — ASN Events

Placental mitochondrial dysfunction in pregnancies complicated by asthma (#214)

Zainab Ali 1 , Nicolette A Hodyl 1 , Annette Osei-Kumah 1 , Zarqa Saif 1 , Vicki L Clifton 1
  1. Robinson institute, Elizabeth Vale, SA, Australia

Asthma is a common chronic respiratory condition complicating around 12% of pregnancies in Australia. Neonates born to mothers with asthma often display reduced growth or intrauterine growth restriction if mothers have an asthma exacerbation during pregnancy. This most frequently occurs when mothers do not use inhaled corticosteroids to treat their asthma. The mechanisms contributing to poor fetal growth in pregnancies complicated by asthma are unclear, however mitochondrial dysfunction has recently been proposed to play a role. For example, in an in vitro model of rat embryo culture, inhibition of mitochondrial function decreased embryo development, gene expression and once implanted, fetal and placental growth were altered. The aim of this study was to characterize the expression of key mitochondrial genes in placentae from pregnancies complicated by asthma according to inhaled corticosteroid use and from healthy control pregnancies. Placentae were collected within 45 minutes of delivery and snap frozen for RNA and protein analysis. Asthma was associated with an increase in placental malate dehydrogenase-2 (MDH2) expression relative to controls irrespective of inhaled corticosteroid use. The abundance of placental Catechol-O-methyltransferase (COMT) and Coproporphyrinogen oxidase (CPOX) was increased with maternal asthma when no inhaled corticosteroids were used however were reduced to levels equivalent to controls when inhaled corticosteroids were used during pregnancy. The alterations in these genes can induce reactive oxygen species (ROS) production in the cell. The normalization of placental CPOX and COMT expression with inhaled corticosteroids may protect the placenta from increased ROS production, ultimately allowing the fetus to grow normally in presence of maternal asthma. The identification of mitochondrial dysfunction in asthmatic pregnancies may aid in understanding pathways leading to altered fetal growth, and therefore lead to the identification of novel targets for intervention during pathological pregnancies.