Altered activity of lysophospholipase D, which produces bioactive lysophosphatidic acid and choline, in serum from women with pathological pregnancy.
Altered activity of lysophospholipase D, which produces bioactive lysophosphatidic acid and choline, in serum from women with pathological pregnancy.
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病理性妊娠妇女血清中溶血磷脂酶 D 的活性发生改变，该酶可产生具有生物活性的溶血磷脂酸和胆碱。
DOI：
10.1093/molehr/gap017
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发表时间：
2009
影响因子：
4
通讯作者：
H. Kanzaki
中科院分区：
文献类型：
--
作者：
A. Tokumura;T. Kume;S. Taira;K. Yasuda;H. Kanzaki
脂质代谢的改变与人类异常妊娠有关，如先兆子痫和早产，并可能导致胎儿丢失。与病理性妊娠相关的全身性多因素综合征的发病和进展的致病因素是氧化低密度脂蛋白，其活性身份被假定为溶血磷脂酸（LPA）。我们以前发现，LPA是由血浆溶血磷脂酶D（lysoPLD）的自分泌运动因子，肿瘤细胞的运动刺激蛋白的活性细胞外产生。在这项研究中，一个方便的测定的基础上释放的胆碱从内源性底物或外源性溶血磷脂酰胆碱（LPC）用于比较血清中的lysoPLD活性正常和异常妊娠患者。发现血清胆碱产生活性主要是由于自分泌运动因子，并依赖于其稀释率。在早产和先兆子痫患者中，血清lysoPLD活性对外源性LPC的低稀释依赖性和对内源性底物的高lysoPLD活性之间存在一定的相关性。正常妊娠组与病理妊娠组血清LPC水平无显著性差异。这些结果表明，通过lysoPLD活性的生物活性LPA的产生通过一种未知的机制升高，该机制可能与内源性底物LPC的可用性增加有关，但与其在人血清中的浓度无关。如果体内病理性妊娠时血液循环中LPA水平升高，则可能在早产或先兆子痫患者全身血管功能障碍的诱导和/或进展中发挥作用。
Altered lipid metabolism is associated with human abnormal pregnancy, such as pre-eclampsia and preterm labor, and potentially leads to fetus loss. A causative factor for the onset and progress of the systemic multifactorial syndromes associated with the pathological pregnancy is oxidized low-density lipoprotein, an active identity of which was postulated to be lysophosphatidic acid (LPA). We previously found that LPA is produced extracellularly by plasma lysophospholipase D (lysoPLD) activity of autotaxin, a tumor cell motility-stimulating protein. In this study, a convenient assay based on the choline released from endogenous substrate or exogenous lysophosphatidylcholine (LPC) was used for comparison of serum lysoPLD activity among patients with normal and abnormal pregnancy. The serum choline-producing activity was found to be mainly due to autotaxin, and dependent on its dilution rate. There was some association between low dilution dependency of serum lysoPLD activity toward an exogenous LPC and high lysoPLD activity toward endogenous substrates in cases of patients with preterm labor and pre-eclampsia. However, there was no difference in the serum level of LPC between women with normal pregnancy and those with pathological pregnancy. These results indicate that production of bioactive LPA by lysoPLD activity is elevated by an unknown mechanism that may be related to increased availability of endogenous substrates LPC, but not its concentration in human serum. If the level of LPA in blood circulation is elevated in the pathological pregnancies in vivo, it may play a role in induction and/or progression of systemic vascular dysfunction seen patients with preterm labor or pre-eclampsia.
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DOI：
--
发表时间：
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期刊：
The Journal of biological chemistry
影响因子：
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发表时间：
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