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植入前小鼠胚胎中空泡的扩张:细胞外钠和氯的作用及其可能的顶端进入途径。

Blastocoel expansion in the preimplantation mouse embryo: role of extracellular sodium and chloride and possible apical routes of their entry.

作者信息

Manejwala F M, Cragoe E J, Schultz R M

机构信息

Department of Biology, University of Pennsylvania, Philadelphia 19104-6018.

出版信息

Dev Biol. 1989 May;133(1):210-20. doi: 10.1016/0012-1606(89)90312-6.

DOI:10.1016/0012-1606(89)90312-6
PMID:2540052
Abstract

The trophectoderm of the mouse blastocyst is a fluid transporting epithelium that is responsible for generating a fluid-filled cavity called the blastocoel. Vectorial transport of ions from the medium into the blastocoel generates an osmotic gradient that drives fluid across this epithelium. We report here that substitution of Na+ or Cl-, but not K+, in the medium halves the rate of blastocoel expansion in the mouse blastocyst. Entrance of Na+ into the trophectoderm may involve several routes, since both blastocoel expansion and 22Na+ uptake are decreased in the presence of the highly specific Na+/H+ exchanger inhibitor, 5-(N-ethyl-N-isopropyl)amiloride, and to a lesser extent with the amiloride-sensitive Na+-channel blocker, benzamil. Uptake of 22Na+ manifests saturation kinetics as a function of extracellular Na+ concentration, whereas uptake of 36Cl- is linear. Furthermore, neither 4,4-diisothiocyanostilbene-2,2-disulfonic acid, which is an inhibitor of the Cl-/HCO3- exchanger, nor 2-(3,4-dichlorobenzyl)-5-nitrobenzoic acid, which is a Cl- -channel blocker, affect either blastocoel expansion or 36Cl- uptake. These results suggest that Na+ entry into the mouse blastocyst is carrier-mediated and probably involves several routes that include the Na+/H+ exchanger and possibly the Na+-channel. Chloride entry, however, may not be carrier-mediated and may occur through a paracellular route, i.e., between the trophectodermal cells.

摘要

小鼠囊胚的滋养外胚层是一种负责产生称为囊胚腔的充满液体的腔的液体运输上皮细胞。离子从培养基向囊胚腔的矢量运输产生了驱动液体穿过该上皮细胞的渗透梯度。我们在此报告,培养基中Na⁺或Cl⁻的替代,但不是K⁺,会使小鼠囊胚中囊胚腔扩张的速率减半。Na⁺进入滋养外胚层可能涉及多种途径,因为在存在高度特异性的Na⁺/H⁺交换抑制剂5-(N-乙基-N-异丙基)氨氯吡咪时,囊胚腔扩张和²²Na⁺摄取均减少,而在对氨氯吡咪敏感的Na⁺通道阻滞剂苄甲咪存在时,减少程度较小。²²Na⁺的摄取表现出作为细胞外Na⁺浓度函数的饱和动力学,而³⁶Cl⁻的摄取是线性的。此外,Cl⁻/HCO₃⁻交换抑制剂4,4-二异硫氰基芪-2,2-二磺酸和Cl⁻通道阻滞剂2-(3,4-二氯苄基)-5-硝基苯甲酸均不影响囊胚腔扩张或³⁶Cl⁻摄取。这些结果表明,Na⁺进入小鼠囊胚是载体介导的,可能涉及包括Na⁺/H⁺交换器以及可能的Na⁺通道在内的多种途径。然而,Cl⁻的进入可能不是载体介导的,可能通过旁细胞途径发生,即在滋养外胚层细胞之间。

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