Berdyshev E V, Schmid P C, Dong Z, Schmid H H
The Hormel Institute, University of Minnesota, 801 16th Avenue NE, Austin, MN 55912, USA.
Biochem J. 2000 Mar 1;346 Pt 2(Pt 2):369-74.
It has long been known that N-acylethanolamine phospholipids [N-acylphosphatidylethanolamine (N-acyl PE)] and N-acylethanolamines (NAEs) accumulate in mammalian tissues undergoing degenerative membrane changes associated with necrosis. Here we studied the effects of stress factors (UVB irradiation and serum deprivation) on the endogenous levels of N-acyl PE and NAE in mouse epidermal JB6 P(+) cells. We found that 16:0, 18:0, 18:1,n-9 and 18:1,n-7 are the predominant amide-linked fatty acids in both N-acyl PE and NAE in these cells. UVB irradiation and serum deprivation resulted in significantly increased levels of N-acyl PE and NAE, especially 18:1, n-9 N-acyl PE and NAE. UVB challenge increased the cellular content of anandamide (20:4,n-6 NAE), but this increase was the lowest of all NAEs measured. Serum deprivation resulted in a decreased cellular anandamide level, as well as a decrease in 20:4,n-6 N-acyl PE. Interestingly, the replacement of serum-free medium with medium containing 5% (v/v) fetal calf serum after 36 h of serum deprivation restored N-acyl PE and NAE levels almost completely within 4-8 h. These data suggest the involvement of N-acyl PE and NAE in cellular responses to stress.
长期以来,人们一直知道N-酰基乙醇胺磷脂[N-酰基磷脂酰乙醇胺(N-酰基PE)]和N-酰基乙醇胺(NAEs)在经历与坏死相关的退行性膜变化的哺乳动物组织中积累。在此,我们研究了应激因素(UVB照射和血清剥夺)对小鼠表皮JB6 P(+)细胞中N-酰基PE和NAE内源性水平的影响。我们发现,16:0、18:0、18:1,n-9和18:1,n-7是这些细胞中N-酰基PE和NAE中主要的酰胺连接脂肪酸。UVB照射和血清剥夺导致N-酰基PE和NAE水平显著升高,尤其是18:1,n-9 N-酰基PE和NAE。UVB刺激增加了花生四烯乙醇胺(20:4,n-6 NAE)的细胞含量,但这种增加在所有测量的NAEs中是最低的。血清剥夺导致细胞花生四烯乙醇胺水平降低,以及20:4,n-6 N-酰基PE减少。有趣的是,在血清剥夺36小时后,用含有5%(v/v)胎牛血清的培养基替换无血清培养基,在4-8小时内几乎完全恢复了N-酰基PE和NAE水平。这些数据表明N-酰基PE和NAE参与了细胞对应激的反应。