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首页> 外文期刊>Journal of Leukocyte Biology: An Official Publication of the Reticuloendothelial Society >Regulation of cytosolic phospholipase A2alpha by hsp90 and a p54 kinase in okadaic acid-stimulated macrophages.
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Regulation of cytosolic phospholipase A2alpha by hsp90 and a p54 kinase in okadaic acid-stimulated macrophages.

机译：hsp90和p54激酶在冈田酸刺激的巨噬细胞中对胞质磷脂酶A2alpha的调节。

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摘要

In resident mouse peritoneal macrophages, group IVA cytosolic phospholipase A(2) (cPLA(2)alpha) mediates arachidonic acid (AA) release and eicosanoid production in response to diverse agonists such as A23187, phorbol myristate acetate, zymosan, and the enterotoxin, okadaic acid (OA). cPLA(2)alpha is regulated by phosphorylation and by calcium that binds to the C2 domain and induces translocation from the cytosol to membranes. In contrast, OA activates cPLA(2)alpha-induced AA release and translocation to the Golgi in macrophages without an apparent increase in calcium. Inhibitors of heat shock protein 90 (hsp90), geldanamycin, and herbimycin blocked AA release in response to OA but not to A23187, PMA, or zymosan. OA, but not the other agonists, induced activation of a cytosolic serine/threonine 54-kDa kinase (p54), which phosphorylated cPLA(2)alpha in in-gel kinase assays and was associated with cPLA(2)alpha in immunoprecipitates. Activation of the p54 kinase was inhibited by geldanamycin. The kinase coimmunoprecipitated with hsp90 in unstimulated macrophages, and OA induced its loss from hsp90, concomitant with its association with cPLA(2)alpha. The results demonstrate a role for hsp90 in regulating cPLA(2)alpha-mediated AA release that involves association of a p54 kinase with cPLA(2)alpha upon OA stimulation.
机译：在常驻小鼠腹膜巨噬细胞中，IVA胞质磷脂酶A（2）（cPLA（2）alpha）组介导花生四烯酸（AA）释放和类花生酸的产生，以响应各种激动剂，例如A23187，佛波肉豆蔻酸乙酸酯，酵母聚糖和肠毒素，冈田酸（OA）。 cPLA（2）alpha受磷酸化作用和钙离子的调节，而钙离子与C2域结合并诱导从胞质溶胶到膜的转运。相反，OA激活cPLA（2）alpha诱导的AA释放和巨噬细胞中向高尔基体的转运，而钙却没有明显增加。热休克蛋白90（hsp90），格尔德霉素和除草霉素的抑制剂可阻止AA对OA的释放，但对A23187，PMA或酵母聚糖不起作用。 OA，但不是其他激动剂，诱导了胞浆丝氨酸/苏氨酸54-kDa激酶（p54）的活化，该酶在凝胶激酶测定中磷酸化了cPLA（2）alpha，并与免疫沉淀物中的cPLA（2）alpha相关。格尔德霉素抑制了p54激酶的活化。该激酶与hsp90在未刺激的巨噬细胞中共免疫沉淀，并且OA诱导其从hsp90中丢失，并与cPLA（2）alpha关联。结果表明hsp90在调节cPLA（2）alpha介导的AA释放中的作用，涉及在OA刺激下将p54激酶与cPLA（2）alpha关联。

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