Murthi Padma, Doherty Vicki L, Said Joanne M, Donath Susan, Brennecke Shaun P, Kalionis Bill
Department of Perinatal Medicine, Pregnancy Research Centre, The Royal Women's Hospital and University of Melbourne, Carlton, Australia.
Mol Hum Reprod. 2006 May;12(5):335-40. doi: 10.1093/molehr/gal037. Epub 2006 Apr 13.
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 (27-35 weeks, n = 13) versus 0.2 +/- 0.06 (36-41 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 (27-36 weeks, n = 11) versus 0.31 +/- 0.02 (36-41 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.
胎儿生长受限（FGR）是一种具有临床意义的妊娠疾病，胎儿在子宫内未能充分发挥其生长潜力。本研究涉及特发性FGR，其常与胎盘功能障碍有关。在此，我们研究了与孕周匹配的对照组相比，早产和足月特发性FGR妊娠中人类胎盘同源盒基因ESX1L的mRNA水平。实时PCR定量显示，对照组胎盘的ESX1L水平在早产和足月之间下降[0.7±0.20（27 - 35周，n = 13）对0.2±0.06（36 - 41周，n = 12），t检验，P < 0.005]。FGR影响的胎盘ESX1L水平显著低于孕周匹配的对照组，早产FGR和足月FGR之间无显著变化[0.32±0.04（27 - 36周，n = 11）对0.31±0.02（36 - 41周，n = 14），t检验，P = 0.82]。多元线性回归分析显示对照组胎盘ESX1L表达迅速下降[每孕周为校准物的0.075倍（95% CI = -0.105至 -0.045，P < 0.0005）]。在FGR影响的胎盘中，ESX1L水平低于孕周匹配的对照组，且ESX1L水平随孕周的下降不显著[每孕周为校准物的0.001倍（95% CI = -0.030至0.010，P < 0.3）]。FGR影响的胎盘和孕周匹配的对照组在妊娠期间ESX1L mRNA水平之间的线性关系显著不同（交互作用的似然比检验，P = 0.0005）。我们的研究结果与ESX1L基因通过影响胎盘功能在胎儿生长控制机制中发挥潜在作用一致。
