Agwu D E, McPhail L C, Wykle R L, McCall C E
Department of Medicine and Biochemistry, Wake Forest University Medical Center, Winston-Salem, NC 27103.
Biochem Biophys Res Commun. 1989 Feb 28;159(1):79-86. doi: 10.1016/0006-291x(89)92407-8.
Quantitation of 1,2-diacylglycerol (AAG), 1-0-alkyl-2-acylglycerol (EAG) and phosphatidic acid (PA) was conducted in polymorphonuclear leukocytes (PMN) labeled with 1-0-[3H]alkyl-2-acyl-GPC following stimulation with 1 microM fMLP using Coomassie blue staining and densitometry. At 5s AAG and PA increased by 80% and 107%, respectively, over controls. The accumulation of PA, which reached a maximum by 30s, was higher than AAG by 302% at 5s, and 550% at 30s. EAG accumulation was delayed by 15s following stimulation of PMN. These results show that AAG accumulates before EAG and support the role of AAG in cellular activation, perhaps, via the stimulation of protein kinase C (PKC). EAG may serve to counter the effects of AAG or may itself elicit responses. The high concentrations of PA which accumulate early suggest that PA may be generated by the activation of phospholipase D in PMN stimulated with fMLP.
在用1微摩尔甲酰甲硫氨酰亮氨酰苯丙氨酸(fMLP)刺激后,使用考马斯亮蓝染色和光密度测定法,对标有1-O-[³H]烷基-2-酰基甘油-3-磷酸胆碱(GPC)的多形核白细胞(PMN)中的1,2-二酰基甘油(AAG)、1-O-烷基-2-酰基甘油(EAG)和磷脂酸(PA)进行定量分析。在5秒时,AAG和PA分别比对照组增加了80%和107%。PA的积累在30秒时达到最大值,在5秒时比AAG高302%,在30秒时高550%。PMN受到刺激后,EAG的积累延迟了15秒。这些结果表明,AAG在EAG之前积累,并支持AAG在细胞激活中的作用,可能是通过刺激蛋白激酶C(PKC)。EAG可能起到抵消AAG作用的功能,或者自身引发反应。早期积累的高浓度PA表明,PA可能是由fMLP刺激的PMN中磷脂酶D的激活产生的。