Effect of the tyrosine kinase inhibitor, genistein, on interleukin-1 stimulated PGE2 production in mesangial cells.
Effect of the tyrosine kinase inhibitor, genistein, on interleukin-1 stimulated PGE2 production in mesangial cells.
复制标题
酪氨酸激酶抑制剂金雀异黄素对白细胞介素 1 的作用刺激了系膜细胞中 PGE2 的产生。
DOI：
10.1016/s0006-291x(05)80094-4
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发表时间：
1990
影响因子：
3.1
通讯作者：
Morrison,AR
中科院分区：
文献类型：
--
作者：
Coyne,DW;Morrison,AR
前列腺素的产生和cAMP的形成是确定的IL-1的两个信号通路，尽管它们都不能充分解释IL-1的众多影响。为了研究酪氨酸磷酸化在IL-1信号传导中的作用，我们使用了酪氨酸激酶抑制剂染料木素。在10 ~ 30 μg/ml浓度下，染料木素阻断IL-1刺激的肾小球系膜细胞中前列腺素的生成和前列腺素内过氧化物合酶（PES）的诱导。在加入IL-1数小时后加入染料木素也会阻止pge2的进一步合成。染料木素未能阻断体外PES活性，表明其不是PES抑制剂。总的来说，这些数据表明酪氨酸磷酸化可能是IL-1刺激pge2和PES活性的必要事件，要么直接作为IL-1信号的一部分，要么间接作为血清/PDGF对系膜细胞能力影响的一部分。
Prostaglandin production and cAMP formation are two signaling pathways identified for IL-1, though neither adequately account for the multitude of effects of IL-1. To investigate the role of tyrosine phosphorylation in IL-1 signaling, we used the tyrosine kinase inhibitor, genistein. At 10–30 μg/ml, genistein blocked IL-1 stimulated prostaglandin production and induction of prostaglandin endoperoxide synthase (PES) in glomerular mesangial cells maintained in 10% serum. Addition of genistein hours after IL-1 addition also halted further PGE2synthesis. Genistein failed to block PES activity in vitro, indicating it was not acting as a PES inhibitor. Overall these data suggest that tyrosine phosphorylation may be a required event for IL-1 stimulation of PGE2and PES activity, either directly as part of IL-1 signaling, or indirectly as part of a serum/PDGF competence effect on mesangial cells.