Plasma S1P and Sphingosine are not Different Prior to Pre-Eclampsia in Women at High Risk of Developing the Disease.

Plasma S1P and Sphingosine are not Different Prior to Pre-Eclampsia in Women at High Risk of Developing the Disease.
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DOI:
10.1016/j.jlr.2022.100312
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发表时间:
2023-01
影响因子:
6.5
通讯作者:
Myers, Jenny E.
Myers, Jenny E.
中科院分区:
生物学2区
文献类型:
--
作者:
Johnstone, Edward D.;Westwood, Melissa;Dilworth, Mark;Wray, Jonathan R.;Kendall, Alexandra C.;Nicolaou, Anna;Myers, Jenny E.

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鞘脂如鞘氨醇-1-磷酸(S1P)与先兆子痫的病理生理学有关。我们假设,血浆S1P将增加妇女在高风险发展先兆子痫谁随后发展的疾病。已知低循环胎盘生长因子(PlGF)与先兆子痫的发展相关;因此,我们进一步假设增加的S1P与同时低PlGF相关。这是一项病例对照研究,使用从95名先兆子痫风险增加的妇女收集的妊娠14至24周的储存母体血液样本。妊娠结局分为无并发症、早产先兆子痫(<37周)或足月先兆子痫。提取血浆脂质并通过超高效液相色谱-电喷雾离子化MS/MS分析,以确定S1P和鞘氨醇的浓度。中位血浆S1P为0.339 nmol/ml,中位鞘氨醇为6.77 nmol/l。在随后发生先兆子痫的妇女中,S1P或鞘氨醇的血浆浓度没有差异,胎龄、胎儿性别、种族或预先存在的高血压没有影响。S1P与血浆鞘氨醇浓度呈显著正相关(P <0.0001)。S1P和鞘氨醇与PlGF无相关性。以往的研究表明,血浆S1P可能是先兆子痫的生物标志物。在我们更大规模的研究中,我们未能证明有女性患上这种疾病的风险很高。我们没有显示与疾病的已知生物标志物的关系,这表明S1P不太可能是妊娠后期先兆子痫发展的有用预测因子。
Sphingolipids like sphingosine-1-phosphate (S1P) have been implicated in the pathophysiology of pre-eclampsia. We hypothesized that plasma S1P would be increased in women at high risk of developing pre-eclampsia who subsequently develop the disease. Low circulating placental growth factor (PlGF) is known to be associated with development of pre-eclampsia; so further, we hypothesized that increased S1P would be associated with concurrently low PlGF. This was a case-control study using stored maternal blood samples from 14 to 24 weeks of pregnancy, collected from 95 women at increased risk of pre-eclampsia. Pregnancy outcome was classified as uncomplicated, preterm pre-eclampsia (<37 weeks), or term pre-eclampsia. Plasma lipids were extracted and analyzed by ultraperformance liquid chromatography coupled to electrospray ionization MS/MS to determine concentrations of S1P and sphingosine. Median plasma S1P was 0.339 nmol/ml, and median sphingosine was 6.77 nmol/l. There were no differences in the plasma concentrations of S1P or sphingosine in women who subsequently developed pre-eclampsia, no effect of gestational age, fetal sex, ethnicity, or the presence of pre-existing hypertension. There was a correlation between S1P and sphingosine plasma concentration (P < 0.0001). There was no relationship between S1P or sphingosine with PlGF. Previous studies have suggested that plasma S1P may be a biomarker of pre-eclampsia. In our larger study, we failed to demonstrate there are women at high risk of developing the disease. We did not show a relationship with known biomarkers of the disease, suggesting that S1P is unlikely to be a useful predictor of the development of pre-eclampsia later in pregnancy.
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