Channon J Y, Leslie C C
Department of Pediatrics, National Jewish Center for Immunology and Respiratory Medicine, Denver, Colorado 80206.
J Biol Chem. 1990 Apr 5;265(10):5409-13.
Arachidonoyl-hydrolyzing phospholipase A2 plays a central role in providing substrate for the synthesis of the potent lipid mediators of inflammation, the eicosanoids, and platelet-activating factor. Although Ca2+ is required for arachidonic acid release in vivo and most phospholipase A2 enzymes require Ca2+ for activity in vitro, the role of Ca2+ in phospholipase A2 activation is not understood. We have found that an arachidonoyl-hydrolyzing phospholipase A2 from the macrophage-like cell line, RAW 264.7, exhibits Ca2(+)-dependent association with membrane. The intracellular distribution of the enzyme was studied as a function of the Ca2+ concentration present in homogenization buffer. The enzyme was found almost completely in the 100,000 x g soluble fraction when cells were homogenized in the presence of Ca2+ chelators and there was a slight decrease in soluble fraction activity when cells were homogenized at the level of Ca2+ in an unstimulated cell (80 nM). When cells were homogenized at Ca2+ concentrations expected in stimulated cells (230-450 nM), 60-70% of the phospholipase A2 activity was lost from the soluble fraction and became associated with the particulate fraction in a manner that was partly reversible with EGTA. Membrane-associated phospholipase A2 activity was demonstrated by [3H]arachidonic acid release both from exogenous liposomes and from radiolabeled membranes. With radiolabeled particulate fraction as substrate, this enzyme hydrolyzed arachidonic acid but not oleic acid from membrane phospholipid, and [3H]arachidonic acid was derived from phosphatidylcholine, phosphatidylethanolamine, and phosphatidylinositol/phosphatidylserine. We suggest a mechanism in which the activity of phospholipase A2 is regulated by Ca2+: in an unstimulated cell phospholipase A2 is found in the cytosol; upon receptor ligation the cytosolic Ca2+ concentration increases, and the enzyme becomes membrane-associated which facilitates arachidonic acid hydrolysis.
花生四烯酰水解磷脂酶A2在为炎症强效脂质介质(类花生酸)和血小板活化因子的合成提供底物方面发挥着核心作用。尽管体内花生四烯酸的释放需要Ca2+,并且大多数磷脂酶A2酶在体外活性需要Ca2+,但Ca2+在磷脂酶A2激活中的作用尚不清楚。我们发现,来自巨噬细胞样细胞系RAW 264.7的花生四烯酰水解磷脂酶A2表现出与膜的Ca2+依赖性结合。研究了该酶在匀浆缓冲液中Ca2+浓度作用下的细胞内分布。当细胞在Ca2+螯合剂存在下匀浆时,该酶几乎完全存在于100,000×g可溶性部分,而当细胞在未刺激细胞的Ca2+水平(80 nM)下匀浆时,可溶性部分活性略有下降。当细胞在刺激细胞预期的Ca2+浓度(230 - 450 nM)下匀浆时,60 - 70%的磷脂酶A2活性从可溶性部分丧失,并以部分可被EGTA逆转的方式与颗粒部分结合。通过[3H]花生四烯酸从外源性脂质体和放射性标记膜中的释放证明了膜相关磷脂酶A2活性。以放射性标记的颗粒部分为底物,该酶从膜磷脂中水解花生四烯酸而非油酸,并且[3H]花生四烯酸来自磷脂酰胆碱、磷脂酰乙醇胺和磷脂酰肌醇/磷脂酰丝氨酸。我们提出了一种磷脂酶A2活性受Ca2+调节的机制:在未刺激的细胞中,磷脂酶A2存在于细胞质中;受体结合后,细胞质Ca +浓度增加,该酶与膜结合,这有利于花生四烯酸的水解。