磷脂甲基化：一种调节淋巴细胞有丝分裂的生化信号。
Phospholipid methylation: a biochemical signal modulating lymphocyte mitogenesis.
作者信息
Hirata F, Toyoshima S, Axelrod J, Waxdal M J
出版信息
Proc Natl Acad Sci U S A. 1980 Feb;77(2):862-5. doi: 10.1073/pnas.77.2.862.
Abstract
Phospholipid methylation in murine T lymphocytes but not B cells was stimulated by mitogenic lectins such as concanavalin A and phytohemagglutinin, and the methylation was then returned to the control level by the concomitant activation of phospholipase A2. A parallelism between dose-response curves of concanavalin A for phospholipid methylation and thymidine incorporation was found. Inhibition of either synthesis or degradation of methylated phospholipids resulted in a decrease in the thymidine incorporation. Although prostaglandins such as the E and F series were the main products of arachidonic acid released by phospholipase A2 activation, inhibition of synthesis of these compounds by indomethacin did not reduce the thymidine incorporation significantly. These results suggest that the mitogenesis of murine T lymphocytes is triggered by the activation of both phospholipid methyltransferase(s) and phospholipase A2.
摘要
促有丝分裂凝集素如刀豆球蛋白A和植物血凝素可刺激小鼠T淋巴细胞而非B细胞中的磷脂甲基化，随后通过磷脂酶A2的同时激活，甲基化水平恢复到对照水平。发现刀豆球蛋白A对磷脂甲基化和胸苷掺入的剂量反应曲线具有平行性。甲基化磷脂合成或降解的抑制均导致胸苷掺入减少。尽管前列腺素如E系列和F系列是磷脂酶A2激活释放的花生四烯酸的主要产物，但吲哚美辛对这些化合物合成的抑制并未显著降低胸苷掺入。这些结果表明，小鼠T淋巴细胞的有丝分裂是由磷脂甲基转移酶和磷脂酶A2的激活共同触发的。
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