Prasad C, Mori M, Greeley G H, Edwards R M, Wilber J F, Pegues J
Brain Res. 1985 May 13;334(1):41-6. doi: 10.1016/0006-8993(85)90565-7.
S-adenosyl-L-methionine-dependent methylation of membrane phosphatidylethanolamine to phosphatidylcholine has been shown to exist in a number of tissues including pituitary gland and to play important roles in receptor-mediated functions. The possible role of this phospholipid methylation reaction in pituitary hormone secretion has been studied. To this end, the ability of thyrotropin-releasing hormone (TRH) to release thyrotropin (TSH) and prolactin and the ability of luteinizing hormone-releasing hormone (LH-RH) to release luteinizing hormone (LH) were evaluated after inhibition of pituitary phospholipid methylation. Both TRH and LH-RH stimulated the release of their corresponding pituitary hormone in a dose-dependent manner and this stimulatory effect was inhibited in the presence of phospholipid methylation inhibitors. Non-specific stimulation of TSH release by 55 mM KCl or 0.1 mM veratridine, however, was not affected by the methylation inhibitors. The data suggest that phospholipid methylation may participate in receptor-mediated release of pituitary hormones.
膜磷脂酰乙醇胺依赖S-腺苷-L-甲硫氨酸甲基化生成磷脂酰胆碱的反应已在包括垂体在内的多种组织中被证实存在，并在受体介导的功能中发挥重要作用。人们对这种磷脂甲基化反应在垂体激素分泌中的可能作用进行了研究。为此，在抑制垂体磷脂甲基化后，评估了促甲状腺激素释放激素（TRH）释放促甲状腺激素（TSH）和催乳素的能力，以及促黄体生成素释放激素（LH-RH）释放促黄体生成素（LH）的能力。TRH和LH-RH均以剂量依赖的方式刺激其相应垂体激素的释放，且在存在磷脂甲基化抑制剂的情况下，这种刺激作用受到抑制。然而，55 mM KCl或0.1 mM藜芦碱对TSH释放的非特异性刺激不受甲基化抑制剂的影响。这些数据表明，磷脂甲基化可能参与受体介导的垂体激素释放。
