Transplacental uptake of glucose is decreased in embryonic lethal connexin26-deficient mice.
Transplacental uptake of glucose is decreased in embryonic lethal connexin26-deficient mice.
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DOI：
10.1083/jcb.140.6.1453
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发表时间：
1998-03-23
影响因子：
7.8
通讯作者：
Willecke, K
中科院分区：
文献类型：
--
作者：
Gabriel, HD;Jung, D;Bützler, C;Temme, A;Traub, O;Winterhager, E;Willecke, K
编码间隙连接蛋白connexin26的基因存在靶向纯合子缺陷的小鼠在妊娠早期到妊娠中期的过渡阶段在子宫内死亡。自交精后第10天起，纯合子胚胎发育迟缓，导致交精后第11天左右死亡。除了生长迟缓外，纯合子连接26缺陷胚与野生型幼崽之间没有明显的形态学改变。在性交后第9天，当绒毛膜尿囊胎盘开始发挥功能时，connexin26在卵黄囊上皮、胎盘迷宫区合体滋养细胞I和II之间以及胚胎皮肤中表达较弱。在交媾后第10天，胎盘中connexin26的表达明显强于其他部位。为了分析connexin26在胎盘营养转移中的作用，我们测量了胚胎对不可代谢的葡萄糖类似物3-O-[14C]甲基葡萄糖的摄取，并将其注射到母体尾静脉。在交媾后第10天，有活力的纯合子有缺陷的胚胎积累的放射性仅为相同大小的野生型和杂合子幼崽的约40%。我们得出结论，从母体血液中摄取葡萄糖（可能还有其他营养物质）到缺乏connexin26的小鼠胚胎严重受损，显然不足以支持妊娠中期的快速器官发生。我们的研究结果表明，connexin26缝隙连接通道可能在小鼠胎盘迷宫层合胞滋养细胞I和II之间的母体营养物质和胚胎废物的转移中发挥了重要作用。
Mice that harbor a targeted homozygous defect in the gene coding for the gap junctional protein connexin26 died in utero during the transient phase from early to midgestation. From day 10 post coitum onwards, development of homozygous embryos was retarded, which led to death around day 11 post coitum. Except for growth retardation, no gross morphological alterations were detected between homozygous connexin26-defective embryos and wild-type littermates. At day 9 postcoitum, when chorioallantoic placenta started to function, connexin26 was weakly expressed in the yolk sac epithelium, between syncytiotrophoblasts I and II in the labyrinth region of the placenta, and in the skin of the embryo. At day 10 post coitum, expression of connexin26 in the placenta was much stronger than at the other locations. To analyze involvement of connexin26 in the placental transfer of nutrients, we have measured embryonic uptake of the nonmetabolizable glucose analogue 3-O-[14C]methylglucose, injected into the maternal tail vein. At day 10 post coitum, viable, homozygous connexin26-defective embryos accumulated only ∼40% of the radioactivity measured in wild-type and heterozygous littermates of the same size. We conclude that the uptake of glucose, and presumably other nutrients as well, from maternal blood into connexin26-deficient mouse embryos was severely impaired and apparently not sufficient to support the rapid organogenesis during midgestation. Our results suggest that connexin26 gap junction channels likely fulfill an essential role in the transfer of maternal nutrients and embryonic waste products between syncytiotrophoblast I and II in the labyrinth layer of the mouse placenta.
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DOI：
10.1083/jcb.129.3.805
发表时间：
1995-05
期刊：
The Journal of cell biology
影响因子：
--
作者：
Elfgang C;Eckert R;Lichtenberg-Fraté H;Butterweck A;Traub O;Klein RA;Hülser DF;Willecke K
通讯作者：
Willecke K
影响因子：
64.8
作者：
NICHOLSON, B;DERMIETZEL, R;REVEL, JP
通讯作者：
REVEL, JP
DOI：
10.1083/jcb.119.1.179
发表时间：
1992-10
期刊：
The Journal of cell biology
影响因子：
--
作者：
Meyer RA;Laird DW;Revel JP;Johnson RG
通讯作者：
Johnson RG
DOI：
10.1073/pnas.86.24.10148
发表时间：
1989-12-01
影响因子：
11.1
作者：
DERMIETZEL, R;TRAUB, O;WILLECKE, K
通讯作者：
WILLECKE, K
影响因子：
4.8
作者：
MEDA, P;PEPPER, MS;ORCI, L
通讯作者：
ORCI, L