Ara C, Massimi M, Devirgiliis Conti L
Dipartimento di Biologia di Base ed Applicata, Facoltà di Scienze, Università de L'Aquila, Via Vetoio, 67010, Coppito AQ, Italy.
Cell Mol Life Sci. 2002 Oct;59(10):1758-65. doi: 10.1007/pl00012503.
Gap junctional communication permits the direct exchange of small molecules and ions and has been implicated in tissue homeostasis/metabolite exchange. The lack of gap junctional intercellular communication (GJIC) plays important roles in the promotion and progression of carcinogenesis. In the present study, we demonstrate that treatment of human hepatoma Hep G2 cells with retinoic acid (RA) results in increased amounts and phosphorylation of connexins, their stabilisation in plasma membrane plaques and enhanced GJIC. In cultured fetal hepatocytes, which represent a non-transformed, proliferating and incompletely differentiated liver system, the effects of RA are limited to the establishment of connexin in areas of cell-cell contact and the improvement of GJIC. This suggests that modulation of cell-cell channel communication by RA occurs differently in these two experimental models: while RA is able to revert cell transformation in Hep G2 cells, in fetal hepatocytes it may induce the expression of a more differentiated phenotype.
间隙连接通讯允许小分子和离子的直接交换，并与组织稳态/代谢物交换有关。间隙连接细胞间通讯（GJIC）的缺乏在致癌作用的促进和进展中起重要作用。在本研究中，我们证明用视黄酸（RA）处理人肝癌Hep G2细胞会导致连接蛋白的数量增加和磷酸化，它们在质膜斑块中稳定并增强GJIC。在培养的胎儿肝细胞中，其代表未转化、增殖且未完全分化的肝脏系统，RA的作用仅限于在细胞-细胞接触区域建立连接蛋白并改善GJIC。这表明RA对细胞间通道通讯的调节在这两种实验模型中有所不同：虽然RA能够使Hep G2细胞中的细胞转化恢复正常，但在胎儿肝细胞中它可能诱导更分化表型的表达。
