Placental PHLDA2 expression is increased in cases of fetal growth restriction following reduced fetal movements.
Placental PHLDA2 expression is increased in cases of fetal growth restriction following reduced fetal movements.
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DOI：
10.1186/s12881-016-0279-1
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发表时间：
2016-03-05
影响因子：
--
通讯作者：
John RM
中科院分区：
文献类型：
--
作者：
Janssen AB;Tunster SJ;Heazell AE;John RM
母体感觉胎动减少（RFM）与胎盘功能不全介导的胎儿生长受限（FGR）和死产风险增加相关。在小鼠模型中，母体表达的印迹基因PHLDA 2控制胎儿生长、胎盘发育和胎盘催乳素产生。许多研究还表明，在人类生长受限妊娠中胎盘PHLDA 2表达异常升高。本研究检测了PHLDA 2是否在导致FGR婴儿分娩的RFM妊娠胎盘中异常表达，并探讨了PHLDA 2表达与人胎盘催乳素释放之间的可能关系。绒毛滋养层样品从一组报告RFM的妇女（N = 109）获得，并分析PHLDA 2基因表达。测定母体血清中的hPL水平（N = 74）。胎盘PHLDA 2表达在导致分娩具有FGR的婴儿的RFM妊娠中显著高2.3倍（p < 0.01），在最严重的情况下PHLDA 2表达水平最高。胎盘PHLDA 2表达与母体血清hPL水平相关（r =-0.30，p = 0.008，n = 74），尽管在控制出生体重的多元线性回归分析中未能达到统计学显著性（p = 0.07）。这些结果进一步强调了胎盘PHLDA 2在不良围产期结局中的作用，特别是与RFM相关的FGR。此外，这项研究表明胎盘PHLDA 2表达和胎盘产生hPL之间存在潜在关系，这种关系需要在更大的队列中进一步研究。本文的在线版本（doi：10.1186/s12881-016-0279-1）包含补充材料，可供授权用户使用。
Maternal perception of reduced fetal movements (RFM) is associated with increased risk of fetal growth restriction (FGR) and stillbirth, mediated by placental insufficiency. The maternally expressed imprinted gene PHLDA2 controls fetal growth, placental development and placental lactogen production in a mouse model. A number of studies have also demonstrated abnormally elevated placental PHLDA2 expression in human growth restricted pregnancies. This study examined whether PHLDA2 was aberrantly expressed in placentas of RFM pregnancies resulting in delivery of an FGR infant and explored a possible relationship between PHLDA2 expression and placental lactogen release from the human placenta. Villous trophoblast samples were obtained from a cohort of women reporting RFM (N = 109) and PHLDA2 gene expression analysed. hPL levels were assayed in the maternal serum (N = 74). Placental PHLDA2 expression was significantly 2.3 fold higher in RFM pregnancies resulting in delivery of an infant with FGR (p < 0.01), with highest levels of PHLDA2 expression in the most severe cases. Placental PHLDA2 expression was associated with maternal serum hPL levels (r = −0.30, p = 0.008, n = 74) although this failed to reach statistical significance in multiple linear regression analysis controlling for birth weight (p = 0.07). These results further highlight a role for placental PHLDA2 in poor perinatal outcomes, specifically FGR associated with RFM. Furthermore, this study suggests a potential relationship between placental PHLDA2 expression and hPL production by the placenta, an association that requires further investigation in a larger cohort. The online version of this article (doi:10.1186/s12881-016-0279-1) contains supplementary material, which is available to authorized users.