Department of Molecular and Cellular Biochemistry, The Ohio State University, Columbus, OH 43210, USA.
Mol Neurobiol. 2010 Jun;41(2-3):267-73. doi: 10.1007/s12035-009-8091-y. Epub 2010 Jan 6.
Plasmalogen-selective phospholipase A(2) (PlsEtn-PLA(2)) has been purified from pig brain using multiple column chromatographic procedure. The purified enzyme migrates as a single band on polyacrylamide. It is stimulated by Triton X-100 and inhibited by sodium deoxycholate. Purified PlsEtn-PLA(2) is inhibited by iodoacetate, and this inhibition can be prevented by beta-meracaptoethanol. Treatment of neuronal cell cultures with kainic acid stimulates PlsEtn-PLA(2) activity in a dose-dependent manner, and this stimulation can be blocked by Ly294486, a selective kainic acid receptor antagonist. Activities of PlsEtn-PLA(2) are markedly increased in plasma membrane and synaptosomal plasma membrane fraction prepared from nucleus basalis and hippocampal region of brains from Alzheimer disease patients compared to age-matched controls. It is proposed that accumulation of ceramide and increased expression of cytokines may be responsible for the stimulation of PlsEtn-PLA(2) in Alzheimer disease.
血浆醚脂选择性磷脂酶 A（2）（PlsEtn-PLA（2））已通过多柱色谱程序从猪脑中纯化出来。纯化后的酶在聚丙烯酰胺上迁移为单一带。它受 Triton X-100 刺激，受脱氧胆酸钠抑制。纯化的 PlsEtn-PLA（2）被碘乙酸抑制，而巯基乙醇可以防止这种抑制。用海人酸处理神经元细胞培养物以剂量依赖性方式刺激 PlsEtn-PLA（2）的活性，而这种刺激可被 Ly294486 阻断，Ly294486 是一种选择性海人酸受体拮抗剂。与年龄匹配的对照组相比，来自阿尔茨海默病患者基底核和海马区的血浆膜和突触体血浆膜部分中 PlsEtn-PLA（2）的活性明显增加。据推测，神经酰胺的积累和细胞因子的表达增加可能是阿尔茨海默病中 PlsEtn-PLA（2）刺激的原因。
