Effects of epidermal growth factor versus phorbol ester on kidney epithelial (LLC-PK1) tight junction permeability and cell division.
Effects of epidermal growth factor versus phorbol ester on kidney epithelial (LLC-PK1) tight junction permeability and cell division.
复制标题
表皮生长因子与佛波酯对肾上皮 (LLC-PK1) 紧密连接通透性和细胞分裂的影响。
DOI：
10.1006/excr.1993.1207
复制
发表时间：
1993
影响因子：
3.7
通讯作者：
Mullin,JM
中科院分区：
文献类型：
--
作者：
Soler,AP;Laughlin,KV;Mullin,JM
在极化上皮细胞中，紧密连接（TJ）构成了控制溶质和水的细胞旁流动的屏障。在肾脏LLC-PK 1细胞中，TJ渗透性与溶质（如D-甘露醇）的单向跨上皮通量直接相关，而与跨上皮电阻（TER）呈反比，D-甘露醇对细胞膜转运系统的亲和力可忽略不计。本研究探讨TJ渗透性和细胞增殖LLC-PK 11细胞处理佛波酯，肿瘤促进剂，12-O-十四烷酰基佛波-13-乙酸酯（TPA）或表皮生长因子（EGF），一种无二次致癌作用的有丝分裂原。TPA和EGF均可诱导LLC-PK 1细胞有丝分裂。TPA处理的细胞中的TJ是渗漏的，如TER降低、D-甘露醇通量增加和TJ被钌红渗透所示。与此相反，EGF治疗并没有导致TER的减少，只是稍微增加了D-甘露醇流量，并没有导致钌红渗透的TJ。钌红不能穿透EGF处理的上皮细胞之间的TJ，即使是有丝分裂中的细胞也是如此。因此，这些数据表明，有丝分裂本身并不增加TJ渗透性，这表明在用佛波醇酯促进肿瘤期间观察到的TJ泄漏并不产生于细胞增殖，并且可能与这些细胞的转化明显相关或因果关系。
In polarized epithelia, the tight junctions (TJs) constitute a barrier that controls the paracellular flux of solutes and water. In the renal LLC-PK1cells, the TJ permeability can be correlated directly with the unidirectional transepithelial flux of solutes, such as D-mannitol, which have negligible affinity for cell membrane transport systems, and inversely to the transepithelial electrical resistance (TER). This study investigates TJ permeability and cell proliferation in LLC-PK1cells treated with the phorbol ester, tumor promoter, 12-O-tetradecanoylphorbol-13-acetate (TPA) or with epidermal growth factor (EGF), a mitogen without secondary carcinogenic effects. Both TPA and EGF induced mitogenesis in LLC-PK1cells. The TJs in TPA-treated cells were leaky, as indicated by decreased TER, increased D-mannitol flux, and TJ penetration by ruthenium red. In contrast, EGF treatment did not result in a decrease in TER, only slightly increased the D-mannitol flux, and did not result in ruthenium red penetration of the TJs. This inability of ruthenium red to penetrate TJs between EGF-treated epithelial cells was true even for cells in mitosis. The data therefore indicate that mitogenesis per se does not increase TJ permeability, suggesting that the TJ leakiness observed during tumor promotion with phorbol esters does not arise from cell proliferation and is perhaps associated distinctly with or causal to the transformation of those cells.