Surface binding and uptake of cadmium (Cd2+) by LLC-PK1 cells on permeable membrane supports.
Surface binding and uptake of cadmium (Cd2+) by LLC-PK1 cells on permeable membrane supports.
复制标题
LLC-PK1 细胞在渗透膜支持物上的表面结合和镉 (Cd2) 吸收。
DOI：
10.1007/bf01973681
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发表时间：
1993
影响因子：
6.1
通讯作者：
Lamar,PC
中科院分区：
文献类型：
--
作者：
Prozialeck,WC;Lamar,PC
最近的研究表明，镉对肾上皮细胞株LLC-PK 1的细胞-细胞连接具有相对特异的损伤作用。本研究的目的是研究LLC-PK 1细胞表面结合和摄取Cd 2+与细胞连接破坏的关系。在Falcon细胞培养皿上的LLC-PK 1细胞暴露于含有来自顶室或基底侧室的痕量109 Cd 2+的CdCl 2中，并监测109 Cd 2+的累积长达8 h。通过监测跨上皮电阻来评估细胞-细胞连接的完整性。结果表明，细胞积累的Cd ~（2+）从基底侧室比从顶侧室多3-4倍。Cd 2+从基底外侧室的积累发生在两个阶段：一个快速的，指数阶段，发生在1-2小时，与跨上皮阻力的减少相一致，和一个缓慢的，线性阶段，持续6-8小时。在快速期积累的Cd 2+很容易通过在EGTA中洗涤细胞而去除，这表明大部分Cd 2+结合到细胞表面上的位点。相比之下，大部分的Cd 2+，积累在较慢的阶段不能被EGTA去除，这表明它已经采取了由细胞。进一步的研究表明，快速阶段的镉+积累时，钙离子是在低浓度（0.1 mM），并大大减少时，钙离子是在高浓度（10 mM）。这些结果表明，Cd ~（2+）通过与细胞表面Ca ~（2+）敏感位点相互作用，破坏LLC-PK_1细胞间的连接。
Recent studies have shown that Cd2+has relatively specific damaging effects on cell-cell junctions in the renal epithelial cell line, LLC-PK1. The objective of the present studies was to examine the surface binding and uptake of Cd2+by LLC-PK1cells in relation to the disruption of cell-cell junctions. LLC-PK1cells on Falcon Cell Culture Inserts were exposed to CdCl2containing trace amounts of109Cd2+from either the apical or the basolateral compartments, and the accumulation of109Cd2+was monitored for up to 8 h. The integrity of cell-cell junctions was assessed by monitoring the transepithelial electrical resistance. The results showed that the cells accumulated 3–4 times more Cd2+from the basolateral compartment than from the apical compartment. The accumulation of Cd2+from the basolateral compartment occurred in two phases: a rapid, exponential phase that occurred in 1–2 h and coincided with a decrease in transepithelial resistance, and a slower, linear phase that continued for 6–8 h. The Cd2+that accumulated during the rapid phase was easily removed by washing the cells in EGTA, indicating that most of it was bound to sites on the cell surface. By contrast, most of the Cd2+that accumulated during the slower phase could not be removed by EGTA, indicating that it had been taken up by the cells. Additional studies showed that the rapid phase of Cd2+accumulation was enhanced when Ca2+was present at low concentrations (0.1 mM), and was greatly reduced when Ca2+was present at high concentrations (10 mM). These results suggest that Cd2+damages the junctions between LLC-PK1cells by interacting with Ca2+-sensitive sites on the basolateral cell surface.