Glucocorticoid-induced phospholipase A2-inhibitory proteins mediate glucocorticoid teratogenicity in vitro.
Glucocorticoid-induced phospholipase A2-inhibitory proteins mediate glucocorticoid teratogenicity in vitro.
复制标题
糖皮质激素诱导的磷脂酶 A2 抑制蛋白在体外介导糖皮质激素致畸性。
DOI：
10.1073/pnas.81.4.1140
复制
发表时间：
1984
影响因子：
11.1
通讯作者：
Piddington,R
中科院分区：
文献类型：
--
作者：
Gupta,C;Katsumata,M;Goldman,AS;Herold,R;Piddington,R
地塞米松诱导小牛胸腺合成分子量约等于 55,000 的磷脂酶 A2 抑制蛋白 (PLIP)，以及 A/J 小鼠胸腺和 12 天胚胎 B10 合成分子量为 55,000、40,000、28,000 和 15,000 的 PLIP。老鼠的味觉。制备足够量的小牛胸腺 PLIP 和 15,000 分子量的小鼠胸腺和腭 PLIP，并测试其作为培养的单个小鼠胚胎腭架内侧边缘上皮细胞程序性细胞死亡的抑制剂。所有测试的蛋白质都可以防止内侧边缘上皮的损失，从而在腭培养模型中产生糖皮质激素的致畸作用。 PLIP 和糖皮质激素的这种致畸作用可被花生四烯酸（前列腺素和血栓素的前体）逆转，表明 PLIP 通过抑制磷脂酶 A2 介导糖皮质激素的作用。
Dexamethasone induces the synthesis of a phospholipase A2-inhibitory protein (PLIP) of molecular weight approximately equal to 55,000 from calf thymus and PLIPs of molecular weights 55,000, 40,000, 28,000, and 15,000 from A/J mouse thymus and from 12-day embryonic B10. A mouse palates. Sufficient quantities of calf thymus PLIP and of the 15,000 molecular weight mouse thymus and palate PLIPs were prepared and tested as inhibitors of programmed cell death in the medial-edge epithelium of single mouse embryonic palatal shelves in culture. All of the proteins tested prevent the loss of the medial-edge epithelium and, thus, produce the teratogenic effects of glucocorticoids in the palatal culture model. This teratogenic action of both PLIP and glucocorticoids is reversed by arachidonic acid, the precursor of prostaglandins and thromboxanes, suggesting that PLIP mediates the effects of glucocorticoids by inhibiting phospholipase A2.