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两种连续肾上皮细胞系中牛磺酸转运的适应性调节。

Adaptive regulation of taurine transport in two continuous renal epithelial cell lines.

作者信息

Jones D P, Miller L A, Chesney R W

机构信息

Department of Pediatrics, University of Tennessee, College of Medicine, Memphis.

出版信息

Kidney Int. 1990 Aug;38(2):219-26. doi: 10.1038/ki.1990.189.

DOI:10.1038/ki.1990.189
PMID:2402115
Abstract

Taurine is actively transported by a beta-amino acid transporter located on the proximal tubule apical surface. We have characterized taurine transport into confluent monolayers of two continuous renal epithelial cell lines: LLC-PK1, a cell of porcine proximal tubular origin, and the Madin-Darby canine kidney cell line (MDCK) of distal origin. Taurine uptake is linear up to 90 minutes in LLC-PK1 cells and 180 minutes in MDCK cells. This process is highly dependent upon Na+ as the cation and either Cl- or Br- as the anion. Taurine uptake is inhibited by another beta-amino acid, beta-alanine, to a greater extent than the alpha-analog, L-alanine or other alpha-amino acids. Incubation of cell monolayers with taurine-free medium (0 microM taurine) induces an increase in Na(+)-dependent taurine uptake when compared to cells exposed to standard medium (50 microM taurine). When cells were incubated in medium containing high taurine (500 microM), uptake was decreased as compared to control cells. This adaptive response is evident by 12 hours in both cell lines and is the result of changes in the apparent transport maximum (Jmax) rather than the apparent Km for taurine. The changes in transport observed after manipulation of medium taurine concentration were not associated with differences in taurine efflux. In summary, taurine is transported by a beta-specific, Na-Cl dependent process in both renal epithelial cell lines. Although the factors which regulate taurine transport are not known, an increased transport maximum is observed in cells which have been taurine-starved, and a decreased Jmax is seen in cells supplied with excess taurine.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

牛磺酸由位于近端小管顶端表面的β-氨基酸转运体主动转运。我们已对牛磺酸转运至两种连续肾上皮细胞系的汇合单层细胞中的过程进行了表征:LLC-PK1,一种源自猪近端小管的细胞,以及源自远端的麦氏达比犬肾细胞系(MDCK)。在LLC-PK1细胞中,牛磺酸摄取在长达90分钟内呈线性,在MDCK细胞中则长达180分钟。该过程高度依赖于作为阳离子的Na⁺以及作为阴离子的Cl⁻或Br⁻。与α-类似物L-丙氨酸或其他α-氨基酸相比,另一种β-氨基酸β-丙氨酸对牛磺酸摄取的抑制作用更大。与暴露于标准培养基(50μM牛磺酸)的细胞相比,用无牛磺酸培养基(0μM牛磺酸)孵育细胞单层会诱导Na⁺依赖性牛磺酸摄取增加。当细胞在含有高浓度牛磺酸(500μM)的培养基中孵育时,与对照细胞相比摄取减少。在两种细胞系中,这种适应性反应在12小时时就很明显,并且是表观转运最大值(Jmax)而非牛磺酸的表观Km发生变化的结果。在改变培养基牛磺酸浓度后观察到的转运变化与牛磺酸外排的差异无关。总之,在两种肾上皮细胞系中,牛磺酸通过β特异性、Na-Cl依赖性过程进行转运。尽管调节牛磺酸转运的因素尚不清楚,但在牛磺酸饥饿的细胞中观察到转运最大值增加,而在供应过量牛磺酸的细胞中则观察到Jmax降低。(摘要截断于250字)

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