Facilitative Glucose Transporter Type 1 Is Differentially Regulated by Progesterone and Estrogen in Murine and Human Endometrial Stromal Cells
Facilitative Glucose Transporter Type 1 Is Differentially Regulated by Progesterone and Estrogen in Murine and Human Endometrial Stromal Cells
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DOI：
10.1210/en.2008-1081
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发表时间：
2009-03-01
期刊：
影响因子：
4.8
通讯作者：
Moley, H.
中科院分区：
文献类型：
--
作者：
Frolova, Antonina;Flessner, Lauren;Moley, H.
胚胎着床是激活的胚泡和接受性子宫内膜之间高度同步的事件。这一过程的成功依赖于雌激素(E-2)和孕酮(P-4)的动态相互作用，然而，这种相互作用的细节并不完全清楚。最近的数据表明，E-2和P-4通过影响促进性葡萄糖转运体(GLUT)的表达来调节葡萄糖的利用。在这项研究中，我们使用原代培养系统检测了GLUT1在小鼠和人子宫内膜间质细胞(ESCs)中的表达。我们发现在体外胚胎干细胞蜕膜化过程中，GLUT1的表达增加。P-4上调GLUT1的表达，而E-2下调GLUT1的表达。此外，在ESCs中，P-4增加而E-2减少葡萄糖摄取，这表明GLUT1可能是这些细胞中葡萄糖利用的主要参与者。此外，在用P-4和二丁酰cAMP体外蜕膜化的人ESCs中，GLUT1的表达增加，这表明P-4在人子宫内膜中的作用类似。总之，在多囊卵巢综合征、黄体期缺陷和反复妊娠丢失的患者中，P-4和E-2之间的失衡可能对子宫内膜间质中葡萄糖的利用产生重要影响，因此，可能是这些患者群体中子宫内膜功能障碍和胚胎植入失败的原因。(内分泌学150：1512-1520,2009)
Embryo implantation is a highly synchronized event between an activated blastocyst and a receptive endometrium. The success of this process relies on the dynamic interplay of estrogen (E-2) and progesterone (P-4), however, the details of this interaction are not entirely clear. Recent data implicate E-2 and P-4 in the regulation of glucose utilization by affecting facilitative glucose transporter (GLUT) expression. In this study we examine GLUT1 expression in murine and human endometrial stromal cells (ESCs) using a primary culture system. We show that expression of GLUT1 is increased during ESC decidualization in vitro. P-4 up-regulates, whereas E-2 down-regulates, GLUT1 expression. In addition, P-4 increases and E-2 decreases glucose uptake in ESCs, suggesting that GLUT1 may be a major player in glucose utilization in these cells. Moreover, GLUT1 expression is increased in human ESCs when decidualized in vitro with P-4 and dibutyryl cAMP, suggesting a similar role for P-4 in human endometrium. In conclusion, an imbalance between P-4 and E-2 seen in patients with polycystic ovary syndrome, luteal phase defect, and recurrent pregnancy loss may have a critical impact on glucose utilization in the endometrial stroma, and, thus, may be responsible for endometrial dysfunction and failure of embryo implantation in these patient populations. (Endocrinology 150: 1512-1520, 2009)