Chow S C, Ansotegui I J, Jondal M
Department of Immunology, Karolinska Institute, Stockholm, Sweden.
Biochem J. 1990 May 1;267(3):727-32. doi: 10.1042/bj2670727.
The effect of omega-3, omega-6 and omega-9 unsaturated fatty acids (UFAs) on receptor-mediated Ca2+ entry was investigated in a T-cell line (JURKAT) by using anti-CD3 antibodies (OKT3) to induce intracellular Ca2+ [( Ca2+]i) increase and Ca2+ influx. All the UFAs, as well as Ni2+ ions and 12-O-tetradecanoylphorbol 13-acetate, decreased the OKT3-induced sustained [Ca2+]i increase to basal levels. Although non-esterified fatty acids activate protein kinase C (PKC) [McPhail, Clayton & Snyderman (1984) Science 224, 622-624; Murakami, Chan & Routtenberg (1986) J. Biol. Chem. 261, 15424-15429], studies using H-7 and analysis of the PKC-dependent phosphorylation of 19 and 80 kDa marker substrates ruled out the involvement of PKC in UFA-induced inhibition of Ca2+ entry. Flow-cytometry analysis showed that UFAs do not interfere with antibody-receptor binding. BSA (0.2%, w/v) reversed the effect of UFAs after these fatty acids have decreased the OKT3-induced [Ca2+]i increase to basal levels. The relevance of these findings and possible mechanisms for inhibition by UFAs of receptor-mediated Ca2+ influx were discussed.
通过使用抗CD3抗体（OKT3）诱导细胞内Ca2+（[Ca2+]i）升高和Ca2+内流，研究了ω-3、ω-6和ω-9不饱和脂肪酸（UFA）对T细胞系（JURKAT）中受体介导的Ca2+内流的影响。所有的UFA以及Ni2+离子和12-O-十四酰佛波醇-13-乙酸酯都将OKT3诱导的[Ca2+]i持续升高降低至基础水平。尽管非酯化脂肪酸可激活蛋白激酶C（PKC）[麦克菲尔、克莱顿和斯奈德曼（1984年）《科学》224，622 - 624；村上、陈和劳滕伯格（1986年）《生物化学杂志》261，15424 - 15429]，但使用H - 7以及对19 kDa和80 kDa标记底物的PKC依赖性磷酸化分析排除了PKC参与UFA诱导的Ca2+内流抑制作用。流式细胞术分析表明，UFA不干扰抗体 - 受体结合。在这些脂肪酸将OKT3诱导的[Ca2+]i升高降低至基础水平后，牛血清白蛋白（0.2%，w/v）可逆转UFA的作用。讨论了这些发现的相关性以及UFA抑制受体介导的Ca2+内流的可能机制。
