van Valen F, Keck E, Jürgens H
Universitätskinderklinik, Abt. für Hämatologie und Onkologie, Düsseldorf, FRG.
FEBS Lett. 1989 Jun 5;249(2):271-4. doi: 10.1016/0014-5793(89)80639-8.
Neuropeptide Y (NPY) regulation of intracellular cyclic AMP accumulation was studied in human Ewing's sarcoma cell line, WE-68. NPY inhibited vasoactive intestinal peptide (VIP)- and dopamine-stimulated but not basal cyclic AMP formation. The peptide effect was rapid (less than 2 min), concentration-dependent with a half-maximal effective concentration (EC50) of 8 nM NPY, and maximal inhibition reaching 60-70% with 100 nM NPY. Prior exposure of WE-68 cells to pertussis toxin completely abolished the inhibitory action of NPY. It is concluded that NPY attenuates agonist-stimulated cyclic AMP formation in Ewing's sarcoma WE-68 cells, and may do so via the inhibitory guanine nucleotide regulatory protein of adenylate cyclase.
在人尤因肉瘤细胞系WE-68中研究了神经肽Y（NPY）对细胞内环磷酸腺苷（cAMP）积累的调节作用。NPY抑制血管活性肠肽（VIP）和多巴胺刺激的cAMP形成，但不抑制基础cAMP的形成。该肽的作用迅速（小于2分钟），呈浓度依赖性，半数最大有效浓度（EC50）为8 nM NPY，100 nM NPY时最大抑制率达60 - 70%。将WE-68细胞预先暴露于百日咳毒素可完全消除NPY的抑制作用。结论是，NPY减弱了尤因肉瘤WE-68细胞中激动剂刺激的cAMP形成，并且可能通过腺苷酸环化酶的抑制性鸟嘌呤核苷酸调节蛋白来实现。
