Placental glucose transporter 3 (GLUT3) is up-regulated in human pregnancies complicated by late-onset intrauterine growth restriction.
Placental glucose transporter 3 (GLUT3) is up-regulated in human pregnancies complicated by late-onset intrauterine growth restriction.
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DOI：
10.1016/j.placenta.2013.08.010
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发表时间：
2013-11
期刊：
影响因子：
3.8
通讯作者：
Devaskar, S. U.
中科院分区：
文献类型：
--
作者：
Janzen, C.;Lei, M. Y. Y.;Cho, J.;Sullivan, P.;Shin, B. -C.;Devaskar, S. U.
葡萄糖从母体血液通过胎盘滋养层组织屏障的转运对维持胎儿生长至关重要。在胎儿宫内生长受限（IUGR）所遇到的缺血缺氧情况下，滋养层中葡萄糖转运蛋白（GLUTs）的调节机制尚未得到适当研究。
为了研究特发性IUGR中GLUT1、GLUT3和GLUT4在胎盘中的表达以及GLUT调节的可能机制。
我们分析了来自患有特发性足月IUGR的妇女（n = 10）和孕周匹配的健康对照（n = 10）的胎盘的临床、生化和组织学数据。
我们发现与正常胎盘相比，IUGR胎盘母体侧滋养层（细胞滋养层大于合体滋养层）中GLUT3蛋白表达增加，但GLUT1或GLUT4未发现差异。在正常胎盘和IUGR胎盘之间未观察到GLUT3启动子的甲基化差异。GLUT3表达增加与缺氧诱导因子 - 1α（HIF - 1α）的核浓度增加有关，这表明缺氧可能在GLUT3的上调中起作用。
需要进一步研究以阐明IUGR中GLUT3表达增加是绒毛成熟缺陷的标志，还是滋养层对慢性缺氧的适应性反应。
IUGR患者的滋养层GLUT3表达增加，正如在孕早期的低氧条件下所发现的那样。
Transport of glucose from maternal blood across the placental trophoblastic tissue barrier is critical to sustain fetal growth. The mechanism by which GLUTs are regulated in trophoblasts in response to ischemic hypoxia encountered with intra-uterine fetal growth restriction (IUGR) has not been suitably investigated. To investigate placental expression of GLUT1, GLUT3 and GLUT4 and possible mechanisms of GLUT regulation in idiopathic IUGR. We analyzed clinical, biochemical and histological data from placentas collected from women affected by idiopathic full-term IUGR (n=10) and gestational age-matched healthy controls (n=10). We found increased GLUT3 protein expression in the trophoblast (cytotrophoblast greater than syncytiotrophoblast) on the maternal aspect of the placenta in IUGR compared to normal placenta, but no differences in GLUT1 or GLUT4 were found. No differential methylation of the GLUT3 promoter between normal and IUGR placentas was observed. Increased GLUT3 expression was associated with an increased nuclear concentration of HIF-1α, suggesting hypoxia may play a role in the up-regulation of GLUT3. Further studies are needed to elucidate whether increased GLUT3 expression in IUGR is a marker for defective villous maturation or an adaptive response of the trophoblast in response to chronic hypoxia. Patients with IUGR have increased trophoblast expression of GLUT3, as found under the low-oxygen conditions of the first trimester.
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影响因子：
158.5
作者：
Barker, DJP;Osmond, C;Eriksson, JG
通讯作者：
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发表时间：
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作者：
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