日本質量分析学会 第66回質量分析総合討論会

プログラム

ポスター発表

第4日 5月18日(金)  ポスター会場

神経細胞の蛋白質プロファイルに与えるメマンチンの影響

(1聖マ医大院・疾患プロテオーム・分子病態治療学2聖マ医大院・最新医学研究コース3聖マ医大院・疾患BM・標的分子制御学)
o佐藤政秋1関口潔2佐藤利行1土屋貴大1表山和樹1有戸光美1末松直也1加藤智啓1黒川真奈絵3

Objective: Memantine, a low-affinity NMDA receptor antagonist, is one of primary pharmacological therapies for Alzheimer's disease. To explore novel effects of memantine, we analyzed protein profile change caused by memantine using neuroblastoma cells.
Methods: Human neuroblastoma GIMEN cells were cultured in the presence or absence of 1-100 μM memantine for 48 hours. Effects of memantine on the cell growth were evaluated by counting cell numbers. Proteins were extracted from GIMEN treated with 10 μM memantine and separated by 2D-DIGE. Protein spots of interest were identified by mass spectrometry.
Results: Memantine suppressed the growth of GIMEN in a dose-dependent manner (2-10 μM, 85.5-76.1%, p<0.05; 20-100 μM, 70.0-63.0%, p<0.01). 892 protein spots were detected in the 2D-DIGE of 10 μM memantine-treated and non-treated GIMEN. 13 protein spots showed 1.2-fold or higher intensity by the memantine-treatment than no-treatment, whereas 19 protein spots showed -1.2 (1/1.2)-fold or lower intensity (p<0.05). We identified 6 proteins in 7 out of the 32 spots, which included decreased expression of β-actin, γ-enolase, and glutathione synthetase. These proteins are known to be involved in cell proliferation individually and/or in concert.
Conclusion: Memantine affected protein profiles of GIMEN. Our data suggested a novel effect of memantine to suppress the neuroblastoma cell growth, which may be associated with decreased expression of β-actin, γ-enolase, and glutathione synthetase.