McNulty S, Morgan P J, Thompson M, Davidson G, Lawson W, Hastings M H
Department of Anatomy, University of Cambridge, UK.
Mol Cell Endocrinol. 1994 Feb;99(1):73-9. doi: 10.1016/0303-7207(94)90148-1.
The potential role of phospholipases in mediating melatonin-dependent inhibition of adenylyl cyclase was investigated in pars tuberalis (PT) cultures. The phorbol ester 12-O-tetradecanoylphorbol 13-acetate (TPA) stimulated the release of choline metabolites and increased the transphosphatidylation reaction. The calcium ionophore A23187 stimulated the release of arachidonic acid from cultures. These observations demonstrate phospholipase A and D activities within PT. Phosphatidic acid inhibited forskolin-stimulated production of cyclic AMP both in PT cells and in membrane preparations. This indicates that melatonin could inhibit adenylyl cyclase by increasing phosphatidic acid levels through activation of cellular phospholipases. Melatonin did not stimulate the release of arachidonic acid or choline from PT cultures, nor did it increase intracellular levels of hydrophobic second messengers or stimulate transphosphatidylation. Therefore melatonin does not stimulate phospholipase A and D pathways in PT cells. However, these pathways are present in the PT and their activation could potentially modulate the cellular actions of melatonin.
在结节部(PT)培养物中研究了磷脂酶在介导褪黑素依赖性腺苷酸环化酶抑制中的潜在作用。佛波酯12-O-十四酰佛波醇13-乙酸酯(TPA)刺激胆碱代谢物的释放并增加转磷脂酰化反应。钙离子载体A23187刺激培养物中花生四烯酸的释放。这些观察结果证明了PT内磷脂酶A和D的活性。磷脂酸在PT细胞和膜制剂中均抑制福斯高林刺激的环磷酸腺苷生成。这表明褪黑素可通过激活细胞磷脂酶增加磷脂酸水平来抑制腺苷酸环化酶。褪黑素不会刺激PT培养物中花生四烯酸或胆碱的释放,也不会增加细胞内疏水第二信使的水平或刺激转磷脂酰化。因此,褪黑素不会刺激PT细胞中的磷脂酶A和D途径。然而,这些途径存在于PT中,其激活可能会调节褪黑素的细胞作用。