在滋养层细胞缺氧和乳酸的生产。

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凯HH,朱镕基年代,Tsoi年代

在滋养层细胞缺氧和乳酸的生产。

胎盘。2007 Aug-Sep; 28 (8): 854 - 60。Epub 2007 2月2。

PubMed ID

17275903 (在PubMed

]

文摘

子痫前期的病因是未知的,但被认为是与胎盘缺氧有关。我们之前报道的酶乳酸脱氢酶(LDH)活性和基因表达增加胎盘从preeclamptic怀孕(Tsoi SCM,郑J,徐F,凯HH。微分表达式的乳酸脱氢酶同功酶(LDH)高表达在人类胎盘LDH-A(4)同工酶在先兆子痫的内皮细胞绒毛。胎盘2001;22:317-22]。LDH负责通过糖酵解丙酮酸转化为乳酸。在这项研究中,我们进一步研究了缺氧的作用在初级滋养层细胞和培养的细胞系,JEG3细胞,以获得更好的理解它如何影响乳酸脱氢酶的活动,乳酸生产和监管基因,为子痫前期是一个可能的模型。主要滋养层细胞和JEG3细胞培养在1%的氧气。6、12和24小时,细胞分析LDHA和LDHB同工酶活动,mRNA和蛋白表达与标准培养条件。乳酸测定是在细胞中。缺氧诱导转录因子(HIF-1alpha)蛋白表达证实了免疫印迹。 Two lactate transporters (MCT1 and MCT4) mRNA and protein expression were also studied under hypoxia. Finally, lactate was measured in plasma obtained from patients with severe preeclampsia. Under hypoxic conditions, LDHA mRNA is increased in primary trophoblast cells and JEG3 cells. The HIF-1alpha protein expression is higher in hypoxia-treated JEG3 cells than control. LDHA isozyme activity and its protein expression are increased most significantly at 24h of culture under hypoxia. However, LDHB protein is unchanged while its mRNA is decreased. Lactate secretion from JEG3 cells under hypoxia is increased, as is the lactate levels in the plasma from preeclampsia patients. Of the two lactate transporters studied, MCT4 mRNA and protein level are increased under hypoxia. Our findings support the role of hypoxia in inducing HIF-1alpha activity in trophoblasts and increasing LDH transcription as well as its activity. Higher levels of lactate are produced and secreted which may contribute to the higher lactate levels in plasma of preeclamptic patients. These mechanisms may be important in the pathophysiology of preeclampsia.

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药物靶点

药物	目标	类	生物	药理作用	行动
丙酮酸	Monocarboxylate运输车5	蛋白质	人类	未知的	不可用	细节