Suppr超能文献

培养的牛晶状体上皮细胞中的钠-氯-钾协同转运活性及其在完整牛晶状体中的缺失。

Na(+)-Cl(-)-K+ cotransport activity in cultured bovine lens epithelial cells and its absence in intact bovine lenses.

作者信息

Alvarez L J, Candia O A

机构信息

Department of Ophthalmology, Mount Sinai School of Medicine, New York, NY 10029.

出版信息

Exp Eye Res. 1994 Apr;58(4):479-90. doi: 10.1006/exer.1994.1041.

Abstract

Using 86RbCl, experiments were directed to identify the pathways for K+ entry in bovine lens cells. Experiments were performed on cultured bovine lens epithelial cells, which are known to transform spontaneously in vitro, and on whole bovine lenses. In cultured epithelial monolayers, K+ inflow occurred nearly equally via the Na(+)-K+ pump and a bumetanide-sensitive, Na(+)- and Cl(-)-dependent process. In the simultaneous presence of ouabain and bumetanide, uptake was inhibited by 98%. Significant passive movement of label through K+ channels could not be detected as indicated by the lack of an effect by 5 mM Ba2+. In the presence of ouabain, the concentration of bumetanide producing half-maximal inhibition of K+ uptake was 1.2 x 10(-7) M, a value similar to those of other cell systems in which Na(+)-Cl(-)-K+ cotransport has been demonstrated by various methods. The present system was not affected by attempts to independently perturb cell Ca2+ and cAMP, but K+ uptake was inhibited upon exposure to phorbol esters and to a cell permeable analog of the protein kinase C (PKC) activator diacylglycerol. From experiments with phorbol 12-myristate-13-acetate (PMA), the reduced inflow was attributed to an inhibition of the bumetanide-sensitive pathway. In contrast, treatment with a phorbol ester known not to activate PKC, 4 alpha-phorbol 12,13-didecanoate (4 alpha-PDD), was ineffective; in toto suggesting that the inositol signaling system regulates K+ fluxes in these cells primarily by affecting the rate via a Na(+)-Cl(-)-K+ cotransport mechanism. These results contrasted with those garnered with the intact lens. Lenses were isolated in a bicameral Ussing-type arrangement so that their anterior and posterior aspects could be bathed independently. K+ inflow across the epithelial surface was predominantly mediated by the Na(+)-K+ pump, i.e. ouabain inhibited uptake by 87%. Addition of bumetanide to the anterior bath resulted in an uptake rate not different from that found under control conditions. The present results are consistent with findings in other cell systems which indicate that the Na(+)-Cl(-)-K+ cotransport activity is associated with highly proliferative cells, such as the cultured cells used. It remains to be determined whether activation, or expression, of the cotransporter has a role in the intact lens.

摘要

利用氯化铷进行实验,旨在确定钾离子进入牛晶状体细胞的途径。实验分别在培养的牛晶状体上皮细胞(已知其在体外会自发转化)和完整的牛晶状体上进行。在培养的上皮单层细胞中,钾离子流入几乎同等程度地通过钠钾泵以及一种布美他尼敏感的、依赖钠离子和氯离子的过程发生。在哇巴因和布美他尼同时存在的情况下,摄取被抑制了98%。5 mM钡离子未产生影响,这表明未检测到标记物通过钾离子通道的显著被动移动。在存在哇巴因的情况下,产生钾离子摄取半数最大抑制的布美他尼浓度为1.2×10⁻⁷ M,该值与其他通过各种方法已证明存在钠氯钾共转运的细胞系统的值相似。当前系统不受独立扰动细胞钙离子和环磷酸腺苷的影响,但暴露于佛波酯和蛋白激酶C(PKC)激活剂二酰甘油的细胞可渗透类似物时,钾离子摄取受到抑制。从用佛波醇12 - 肉豆蔻酸酯 - 13 - 乙酸酯(PMA)进行的实验来看,流入减少归因于布美他尼敏感途径的抑制。相比之下,用一种已知不激活PKC的佛波酯4α - 佛波醇12,13 - 十二烷酸酯(4α - PDD)处理无效;总体表明肌醇信号系统主要通过影响钠氯钾共转运机制的速率来调节这些细胞中的钾离子通量。这些结果与在完整晶状体上获得的结果形成对比。晶状体以双室Ussing型装置分离,以便其前表面和后表面可以独立地进行灌注。跨上皮表面的钾离子流入主要由钠钾泵介导,即哇巴因抑制摄取达87%。向前房灌注液中添加布美他尼导致摄取速率与对照条件下的速率无差异。当前结果与其他细胞系统中的发现一致,这些发现表明钠氯钾共转运活性与高度增殖的细胞相关,例如所使用的培养细胞。共转运体的激活或表达在完整晶状体中是否起作用仍有待确定。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验