Hernandez A, Kimball B, Romanchuk G, Mulholland M W
Department of Surgery, University of Michigan, Ann Arbor 48109-0331, USA.
Peptides. 1995;16(5):927-32. doi: 10.1016/0196-9781(95)00059-s.
The ability of PACAP-38 to stimulate morphological development was studied using rat pheochromocytoma PC12 cells. PACAP-38 produced concentration-dependent increases in percentage of cells exhibiting neurite extension. Similar increases were produced by forskolin (28 +/- 2% at 96 h) and 8-bromo cAMP (30 +/- 2%). Vasoactive intestinal peptide and alpha-calcitonin gene-related peptide were without effect. PACAP-38 produced significant increases in PC12 cell cAMP content and inositol phosphate turnover. Intracellular [Ca2+] increased from 169 +/- 14 nM to 560 +/- 58 nM in response to 1 microM PACAP-38. PACAP-stimulated neurite outgrowth was abolished by RpcAMPS, an inhibitor of cAMP-dependent kinases but was unaffected by the protein kinase C antagonist H7.
利用大鼠嗜铬细胞瘤PC12细胞研究了PACAP - 38刺激形态发育的能力。PACAP - 38使表现出神经突延伸的细胞百分比呈浓度依赖性增加。福斯高林（96小时时为28±2%）和8 - 溴环磷腺苷（30±2%）也产生了类似的增加。血管活性肠肽和α - 降钙素基因相关肽无此作用。PACAP - 38使PC12细胞的环磷腺苷含量和肌醇磷酸周转率显著增加。响应1微摩尔PACAP - 38，细胞内[Ca2 + ]从169±14纳摩尔增加到560±58纳摩尔。cAMP依赖性激酶抑制剂RpcAMPS可消除PACAP刺激的神经突生长，但蛋白激酶C拮抗剂H7对其无影响。
