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培养的肾小管细胞中的转运和代谢功能。

Transport and metabolic functions in cultured renal tubule cells.

作者信息

Horster M F, Stopp M

出版信息

Kidney Int. 1986 Jan;29(1):46-53. doi: 10.1038/ki.1986.7.

DOI:10.1038/ki.1986.7
PMID:3515014
Abstract

The study tool of cultured tubule epithelia has been applied to new areas in nephron cell biology, such as the evolution of epithelial membrane asymmetry. Studies utilizing monoclonal antibodies against plasma membrane glycoproteins in MDCK revealed that the development of surface cell polarity is a continuous process requiring intact tight junctions and their electrical resistor function [101]. The role of the junctional complex to establish and maintain distinct membrane protein domains had been suggested earlier from work utilizing the apical aminopeptidase [102] and fluorescent membrane probes [103]. Cultured tubule epithelia lend themselves for the evaluation of cell-specific membrane protein synthesis [104] and antigenic determinants [105]. Human renal epithelia, from normal [106, 107] and defined abnormal kidney [108], have been maintained functional in primary and passage culture [106]. Pathophysiological mechanisms may be examined in cultured tubule epithelia, as shown first [109] by studies on the recovery from ischemic failure, where anoxia and substrate deprivation resulted in cell swelling which was prevented in culture by an oncotic agent. This article has not attempted to give an exhaustive account of the studies in which cultured tubule cells have served as a tool. Instead, the investigations quoted herein represent some principal lines of study, as seen from renal physiology, which may disclose details in culture of complex in vivo phenomena. It was Bernard [110] who, in 1865, suggested that "physiological events must be isolated outside the organism . . . to better understand the deepest associations of the phenomena."

摘要

培养的肾小管上皮细胞这一研究工具已被应用于肾单位细胞生物学的新领域,如上皮细胞膜不对称性的演变。利用针对MDCK细胞膜糖蛋白的单克隆抗体进行的研究表明,表面细胞极性的发展是一个连续的过程,需要完整的紧密连接及其电阻功能[101]。利用顶端氨肽酶[102]和荧光膜探针[103]的研究 earlier 曾提出连接复合体在建立和维持不同膜蛋白结构域方面的作用。培养的肾小管上皮细胞适合用于评估细胞特异性膜蛋白合成[104]和抗原决定簇[105]。来自正常[106, 107]和特定异常肾脏[108]的人肾上皮细胞在原代培养和传代培养中一直保持功能[106]。病理生理机制可以在培养的肾小管上皮细胞中进行研究,正如 first 对缺血性衰竭恢复的研究所表明的那样[109],缺氧和底物剥夺导致细胞肿胀,而在培养中一种渗透剂可防止这种情况发生。本文并未试图详尽列举以培养的肾小管细胞为工具的研究。相反,本文引用的研究代表了一些主要的研究方向,从肾脏生理学角度来看,这些研究可能揭示复杂体内现象在培养中的细节。是伯纳德[110]在1865年提出“生理事件必须在生物体之外分离……以便更好地理解这些现象的最深层次联系”。

相似文献

1
Transport and metabolic functions in cultured renal tubule cells.培养的肾小管细胞中的转运和代谢功能。
Kidney Int. 1986 Jan;29(1):46-53. doi: 10.1038/ki.1986.7.
2
Studies of renal cell function using cell culture techniques.
Am J Physiol. 1980 Jan;238(1):F1-9. doi: 10.1152/ajprenal.1980.238.1.F1.
3
Sodium cotransport processes in renal epithelial cell lines.肾上皮细胞系中的钠协同转运过程。
Miner Electrolyte Metab. 1986;12(1):32-41.
4
Factors affecting the differentiation of epithelial transport and responsiveness to hormones.影响上皮转运分化及对激素反应性的因素。
Fed Proc. 1984 May 15;43(8):2221-4.
5
Primary culture of isolated tubule cells of defined segmental origin.特定节段来源的分离肾小管细胞的原代培养。
Methods Enzymol. 1990;191:409-26. doi: 10.1016/0076-6879(90)91026-3.
6
Expression of sodium pump activity and of transepithelial voltage induced by hormones in cultured cortical collecting tubule cells.培养的皮质集合管细胞中激素诱导的钠泵活性和跨上皮电压的表达。
Miner Electrolyte Metab. 1989;15(3):137-43.
7
Hormonal regulation of Na+ channels in tight epithelia.紧密上皮中钠离子通道的激素调节
Soc Gen Physiol Ser. 1985;39:105-20.
8
[Sodium and water transport mechanisms in amphibian epithelial cells and isolated renal tubules].[两栖动物上皮细胞和离体肾小管中的钠和水转运机制]
J Physiol (Paris). 1975 Jun;71(1):5A-71A.
9
[Intervention of the transtubular oncotic gradient in the reabsorption of sodium by the renal tubule].[经肾小管胶体渗透压梯度对肾小管钠重吸收的干预]
Bull Schweiz Akad Med Wiss. 1967 Dec;23(3):370-5.
10
Sodium entry pathways in renal epithelial cell lines.肾上皮细胞系中的钠进入途径。
Miner Electrolyte Metab. 1986;12(1):42-50.

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Peptide-dependent regulation of epithelial nephron functions.
肽对肾单位上皮功能的依赖性调节。
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Cystine uptake by cultured cells originating from dog proximal tubule segments.源自犬近端肾小管节段的培养细胞对胱氨酸的摄取。
In Vitro Cell Dev Biol. 1990 Feb;26(2):105-12. doi: 10.1007/BF02624100.