Hasler C M, Bennink M R, Trosko J E
Department of Food Science and Human Nutrition, Michigan State University, East Lansing 48824.
Am J Physiol. 1991 Jul;261(1 Pt 1):C161-8. doi: 10.1152/ajpcell.1991.261.1.C161.
The purpose of this investigation was to assess whether alterations in the fatty acid composition of rat liver epithelial (WB-F344) cell phospholipids would modulate gap junction-mediated intercellular communication (GJIC). WB-F344 cells were grown to confluency in culture medium supplemented with one of seven different fatty acids at a concentration of 50 microM for 48 h. Only alpha-linoleate (18:3 n-3) significantly inhibited GJIC. Saturated fatty acids (12:0, 16:0, and 18:0), a monounsaturated fatty acid (18:1 n-9), and n-6 polyunsaturated fatty acids (18:2 and 20:4) did not affect GJIC. The alpha-linolenate-induced inhibition of GJIC was not due to the activation of protein kinase C or intracellular hydroperoxide production, two lipid-dependent parameters previously shown to inhibit GJIC. In addition, alpha-linolenate did not alter membrane fluidity. Although the mechanism by which alpha-linolenate inhibits GJIC is unclear, changes in the fatty acid composition of cell phospholipids may be of critical importance. Subsequent to supplementation with alpha-linolenate, WB-F344 cell phospholipids had reduced 20:4 n-6 and elevated n-3 fatty acids. The results of this investigation emphasize the importance of current research into the influence of lipids on cell function and identify a new mechanism by which gap junctions can be modulated.
本研究的目的是评估大鼠肝上皮（WB - F344）细胞磷脂脂肪酸组成的改变是否会调节间隙连接介导的细胞间通讯（GJIC）。将WB - F344细胞在补充有七种不同脂肪酸之一的培养基中培养至汇合，脂肪酸浓度为50微摩尔，培养48小时。只有α - 亚麻酸（18:3 n - 3）显著抑制GJIC。饱和脂肪酸（12:0、16:0和18:0）、单不饱和脂肪酸（18:1 n - 9）和n - 6多不饱和脂肪酸（18:2和20:4）不影响GJIC。α - 亚麻酸诱导的GJIC抑制不是由于蛋白激酶C的激活或细胞内过氧化氢的产生，这两个先前已证明可抑制GJIC的脂质依赖性参数。此外，α - 亚麻酸不会改变膜流动性。尽管α - 亚麻酸抑制GJIC的机制尚不清楚，但细胞磷脂脂肪酸组成的变化可能至关重要。在用α - 亚麻酸补充后，WB - F344细胞磷脂的20:4 n - 6减少，n - 3脂肪酸增加。本研究结果强调了当前关于脂质对细胞功能影响的研究的重要性，并确定了一种调节间隙连接的新机制。
