Exposure of pulmonary artery endothelial cells to nitrogen dioxide activates phospholipase A1.
Exposure of pulmonary artery endothelial cells to nitrogen dioxide activates phospholipase A1.
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肺动脉内皮细胞暴露于二氧化氮会激活磷脂酶 A1。
DOI：
10.1002/jbt.2570050111
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发表时间：
1990
期刊：
影响因子：
--
通讯作者：
Block,ER
中科院分区：
文献类型：
--
作者：
Bhat,GB;Patel,JM;Block,ER
将猪肺动脉内皮细胞的融合单层暴露于5 ppm NO2（环境污染的有毒成分）24和48小时后，在细胞超声处理物中测定磷脂酶A1、A2和C以及二酰基甘油脂肪酶的活性。（2.25倍）的磷脂酶A1活性在24和48小时NO2暴露的细胞，而磷脂酶A2和C和二酰基甘油脂肪酶的活性在两个时间点与对照细胞相当。当内皮细胞用[3 H]-花生四烯酸预标记，然后暴露于NO2 48小时时，细胞溶血磷脂的计数增加，同时细胞磷脂酰胆碱和磷脂酰乙醇胺的计数减少。这些结果表明NO2暴露导致磷脂酶A1的特异性活化。
Phospholipase A1, A2, and C and diacylglycerol lipase activities were measured in cell sonicates after exposing confluent monolayers of porcine pulmonary artery endothelial cells to 5 ppm NO2, a toxic constituent of environmental pollution, for 24 and 48 hr. There was a significant increase (2.25‐fold) in phospholipase A1activity in 24 and 48 hr NO2‐exposed cells, whereas activities of phospholipases A2and C and diacylglycerol lipase were comparable to control cells at both time points. When endothelial cells were prelabeled with [3H]‐arachidonic acid and then exposed to NO2for 48 hr, increased counts were recovered from cell lysophospholipids with concomitant decreased recovery of counts from cell phosphatidylcholine and phosphatidylethanolamine. These results demonstrate that NO2exposure results in specific activation of phospholipase A1.