Regulation of T84 cell monolayer permeability by insulin-like growth factors.
Regulation of T84 cell monolayer permeability by insulin-like growth factors.
复制标题
胰岛素样生长因子对 T84 细胞单层通透性的调节。
DOI：
10.1152/ajpcell.1992.262.1.c207
复制
发表时间：
1992
期刊：
影响因子：
--
通讯作者：
Riley,NE
中科院分区：
文献类型：
--
作者：
McRoberts,JA;Riley,NE
当在可渗透的支持物上生长时，T84人结肠上皮细胞系形成极化单层培养物，相邻细胞之间具有高电阻紧密连接。添加胰岛素样生长因子（IGF）I或II的基底侧，但不是已建立的单层的顶膜侧引起剂量依赖性的跨上皮阻力下降超过4天的时间。IGF-I比IGF-II更有效，半最大有效浓度分别为0.7和2.2 nM。IGF-I和IGF-II均导致Na+和细胞外空间标记物甘露醇的跨上皮通量率平行增加，表明电阻降低是由于通过紧密连接调节的细胞旁途径的渗透性增加。同时加入放线菌酮防止电阻下降，这意味着蛋白质合成是必要的IGF对细胞旁通透性的影响。用IGF处理单层细胞产生了一个微妙的凝聚的连接周围的肌动蛋白环可视化使用罗丹明标记鬼笔环肽。这些结果表明，IGF-I和-II通过受体介导的过程，可能涉及蛋白质合成和细胞骨架结构的变化调节T84细胞单层的细胞旁通透性。
When grown on permeable supports, the T84 human colonic epithelial cell line forms polarized monolayer cultures with high-resistance tight junctions between adjacent cells. Addition of either insulin-like growth factor (IGF) I or II to the basolateral but not the apical membrane side of established monolayers caused a dose-dependent decrease in transepithelial resistance over a 4-day period. IGF-I was more potent than IGF-II, with half-maximally effective concentrations of 0.7 and 2.2 nM, respectively. Both IGF-I and -II caused a parallel increase in the transepithelial flux rates for Na+ and the extracellular space marker, mannitol, demonstrating that the decrease in electrical resistance was due to increased permeability through the tight junction-regulated paracellular pathway. Simultaneous addition of cycloheximide prevented the decline in electrical resistance, implying that protein synthesis is necessary for the effect of IGF on paracellular permeability. Treatment of monolayers with IGF produced a subtle condensation of the perijunctional actin ring as visualized using rhodamine-labeled phalloidin. These results demonstrate that IGF-I and -II regulate the paracellular permeability of T84 cell monolayers through a receptor-mediated process that probably involves changes in protein synthesis and cytoskeletal structure.