Grove R I, Willis W D, Pratt R M
Biochem Biophys Res Commun. 1983 Jan 14;110(1):200-7. doi: 10.1016/0006-291x(83)91280-9.
Dexamethasone (DEX), a glucocorticoid which induces cleft palate, causes marked alterations in the synthesis and degradation of phosphatidylinositol (PI) but not phosphatidylcholine in an established fibroblastic cell line derived from a human embryonic palate. Incorporation of radiolabeled inositol into phosphatidylinositol as well as degradation of prelabeled phosphatidylinositol is stimulated by DEX. The dose-response curves for the DEX-induced effect on PI synthesis and DEX-induced inhibition of cell proliferation are nearly identical, with the maximal responses occurring at 10(-8)M DEX. Our results suggest that DEX-induced inhibition of human embryonic palatal mesenchyme cell proliferation and alterations in synthesis and degradation of phosphatidylinositol are related.
地塞米松(DEX)是一种可诱发腭裂的糖皮质激素,在源自人胚胎腭部的成纤维细胞系中,它会引起磷脂酰肌醇(PI)合成与降解的显著变化,但不会引起磷脂酰胆碱的类似变化。DEX可刺激放射性标记的肌醇掺入磷脂酰肌醇以及预标记的磷脂酰肌醇的降解。DEX对PI合成的诱导作用和DEX对细胞增殖的抑制作用的剂量反应曲线几乎相同,最大反应出现在10^(-8)M DEX时。我们的结果表明,DEX诱导的人胚胎腭间充质细胞增殖抑制与磷脂酰肌醇合成和降解的变化有关。