从转基因动物培养的肾小管细胞。

G Friedlander, I Runembert, F Vrtovsnik, F Terzi
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引用次数: 9

摘要

转基因动物肾小管细胞的培养为在严格控制的条件下进行生物化学、细胞生物学和生理学研究提供了机会。原代培养或细胞系均可使用。通过从敲除小鼠获得的近端小管细胞原代培养的两个例子,获得了有关蛋白质功能的重要信息。缺乏在再生和培养过程中正常在小管细胞中重新表达的中间丝蛋白的小鼠在基础条件下具有正常的小管功能。从这些动物生长的近端细胞表现出钠-葡萄糖共运输活性的缺陷,很可能与顶端膜中转运蛋白的二聚体/单体比例的改变有关。这些改变在急性肾小管坏死后恢复期的肾小管功能方面可能是重要的。对于缺乏HNF-1的小鼠,情况则截然不同,HNF-1是一种参与多种基因转录的反激活因子。这些动物患有严重的范可尼综合征,与近端转运蛋白表达减少有关,包括钠-葡萄糖(SGLT2)和钠-磷酸钠(NPT1)共转运蛋白的异构体。虽然在分离的小管中观察到转运缺陷,但在培养的近端细胞中不再明显,因为这些同种异构体的表达在培养条件下受到抑制。这些观察结果说明了转基因动物肾脏功能体外模型研究的兴趣和局限性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Renal tubular cells cultured from genetically modified animals.

The culture of renal tubular cells from genetically modified animals opens the opportunity of biochemical, cell biology and physiological studies under strictly controlled conditions. Either primary cultures or cell lines can be used. Through two examples of primary cultures of proximal tubular cells obtained from knock-out mice, important information about the function of proteins were obtained. Mice lacking vimentin, an intermediate filament normally reexpressed in tubular cells during regeneration and culture, have a normal tubular function under basal conditions. Proximal cells grown from these animals exhibit a defect in sodium-glucose cotransport activity, most likely related to alterations in the dimer/monomer ratio of the transporter in the apical membranes. These alterations may be important in terms of tubular function during the recovery phase following acute tubular necrosis. The situation is strikingly different with regard to mice lacking HNF-1, a transactivator involved in the transcription of multiple genes. These animals suffer from severe Fanconi syndrome related to decreased expression of proximal transporters including isoforms of sodium-glucose (SGLT2) and sodium-phosphate (NPT1) cotransporters. Whereas transport defects are observed in isolated tubules, they are no longer apparent in cultured proximal cells because the expression of these isoforms is suppressed under culture conditions. These observations illustrate the interest and limits of the in vitro models for studying renal function in transgenic animals.

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