Mol. Hum. Reprod. Advance Access originally published online on April 13, 2006
Molecular Human Reproduction 2006 12(5):335-340; doi:10.1093/molehr/gal037
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Homeobox gene ESX1L expression is decreased in human pre-term idiopathic fetal growth restriction
1Department of Perinatal Medicine, Pregnancy Research Centre, 2Department of Obstetrics and Gynaecology, The Royal Womens Hospital and University of Melbourne, Carlton and 3Clinical Epidemiology and Biostatistics Unit, Murdoch Childrens Research Institute & University of Melbourne Department of Paediatrics, The Royal Childrens Hospital, Parkville, Victoria, Australia
4 To whom correspondence should be addressed at: Department of Perinatal Medicine, Pregnancy Research Centre, Royal Womens Hospital, 132 Grattan Street, Carlton, Victoria 3053, Australia. E-mail: bill.kalionis{at}rwh.org.au
Fetal growth restriction (FGR) is a clinically significant pregnancy disorder in which the fetus fails to achieve its full growth potential in utero. This study involved idiopathic FGR, which is frequently associated with placental dysfunction. Here, we investigated mRNA levels of the human placental homeobox gene ESX1L in pre-term and term idiopathic FGR pregnancies compared with gestation-matched controls. Real-time PCR quantitation showed ESX1L levels in control placentae decreased between pre-term and term [0.7 ± 0.20 (2735 weeks, n = 13) versus 0.2 ± 0.06 (3641 weeks, n = 12), t-test, P < 0.005]. ESX1L levels in FGR-affected placentae were significantly lower than in gestation-matched controls, and there was no significant change between pre-term FGR and term FGR [0.32 ± 0.04 (2736 weeks, n = 11) versus 0.31 ± 0.02 (3641 weeks, n = 14), t-test, P = 0.82]. Multiple linear regression analysis revealed a rapid decline in ESX1L expression in control placentae [0.075-fold of the calibrator for each week of gestation (95% CI = 0.105 to 0.045, P < 0.0005)]. In FGR-affected placentae, ESX1L levels were lower than in gestation-matched controls, and the decline in ESX1L levels with gestation was not significant [0.001-fold of the calibrator for each week of gestation (95% CI = 0.030 to 0.010, P < 0.3]. The linear relationship between ESX1L mRNA levels in FGR-affected placentae and gestation-matched controls during gestation was significantly different (likelihood ratio test for interaction, P = 0.0005). Our findings were consistent with a potential role for the ESX1L gene within the growth control mechanism of the fetus, through its effect on placental function.
Key words: ESX1L/fetal growth restriction/homeobox/IUGR
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