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母体/新生儿血管内皮生长因子C936T相互作用及其对先兆子痫风险、严重程度和预后的影响,以及对母体血管生成特征的影响。

Maternal/newborn VEGF-C936T interaction and its influence on the risk, severity and prognosis of preeclampsia, as well as on the maternal angiogenic profile.

作者信息

Procopciuc Lucia Maria, Caracostea Gabriela, Zaharie Gabriela, Stamatian Florin

机构信息

Department of Medical Biochemistry and.

出版信息

J Matern Fetal Neonatal Med. 2014 Nov;27(17):1754-60. doi: 10.3109/14767058.2014.942625. Epub 2014 Jul 28.

Abstract

OBJECTIVE

To analyze the influence of maternal/newborn vascular endothelial growth factor (VEGF)-CT936 interaction as a modulating factor in preeclampsia as well as its influence on the maternal angiogenic balance.

METHODS

Seventy pairs of preeclamptic women/newborns and 94 pairs of normal pregnant mothers/newborns were genotyped using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). Serum VEGF and soluble VEGF receptor-1 (sVEGFR-1) levels were measured using ELISA.

RESULTS

The risk to develop mild (odds ratio; OR: 3.79, p = 0.008) and severe (OR: 2.94, p = 0.037) preeclampsia being increased in association with the CT936-VEGF genotype and increased in severe preeclampsia to 6.07 (p = 0.03) if the women were carriers of the homozygous TT936-VEGF genotype. The presence of the VEGF-T936 allele in both the mother and the newborn significantly increases the risk of pregnancy-induced hypertension (PIH), mild and severe preeclampsia. If both the mothers and newborns were carriers of the VEGF-T936 allele, significantly lower VEGF and higher sVEGFR-1 levels were observed for all types of preeclampsia. Pregnant women with PIH and severe preeclampsia delivered at a significantly earlier gestational age neonates with a significantly lower birth weight if both the preeclamptic mothers and their newborns were carriers of the VEGF-T936 allele.

CONCLUSIONS

Our study suggests the role of maternal/fetal VEGF-CT936 polymorphism as a modulating factor in preeclampsia, which affects the angiogenic balance in preeclamptic mothers, as well as their pregnancy outcome.

摘要

目的

分析母胎血管内皮生长因子(VEGF)-CT936相互作用作为子痫前期调节因子的影响及其对母体血管生成平衡的影响。

方法

采用聚合酶链反应-限制性片段长度多态性(PCR-RFLP)对70对子痫前期妇女/新生儿和94对正常孕妇/新生儿进行基因分型。采用酶联免疫吸附测定法(ELISA)检测血清VEGF和可溶性VEGF受体-1(sVEGFR-1)水平。

结果

与CT936-VEGF基因型相关,发生轻度子痫前期(比值比;OR:3.79,p = 0.008)和重度子痫前期(OR:2.94,p = 0.037)的风险增加,若妇女为纯合子TT936-VEGF基因型携带者,则重度子痫前期风险增至6.07(p = 0.03)。母亲和新生儿中均存在VEGF-T936等位基因会显著增加妊娠高血压(PIH)、轻度和重度子痫前期的风险。若母亲和新生儿均为VEGF-T936等位基因携带者,则所有类型子痫前期患者的VEGF水平显著降低,sVEGFR-1水平显著升高。如果子痫前期母亲及其新生儿均为VEGF-T936等位基因携带者,PIH和重度子痫前期孕妇分娩时的孕周显著提前,新生儿出生体重显著降低。

结论

我们的研究表明母胎VEGF-CT936多态性作为子痫前期的调节因子发挥作用,影响子痫前期母亲的血管生成平衡及其妊娠结局。

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