A GLUCOCORTICOID RECEPTOR IN FETAL MOUSE - ITS RELATIONSHIP TO CLEFT-PALATE FORMATION
A GLUCOCORTICOID RECEPTOR IN FETAL MOUSE - ITS RELATIONSHIP TO CLEFT-PALATE FORMATION
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DOI：
10.1002/tera.1420210106
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发表时间：
1980-01-01
期刊：
影响因子：
--
通讯作者：
HACKNEY, JF
中科院分区：
文献类型：
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作者：
HACKNEY, JF
研究了胎鼠组织中可能导致腭裂形成的糖皮质激素结合受体。胎鼠头部含有一种可溶性成分，其在体外以高亲和力结合糖皮质激素曲安奈德。该结合组分以小的有限量存在。其他糖皮质激素与曲安奈德竞争结合位点，其方式与其作为腭裂致畸剂的效力等级一致。几种盐皮质激素和孕激素在体外给药时也会竞争，但在体内给药时不会。在3种小鼠品系A/J、C3 H和C57 BL中测定了曲安奈德结合，这些小鼠品系以腭裂对可的松的敏感性降序排列。未发现这些菌株胎儿中可的松腭裂易感性与曲安奈德结合亲和力或结合量呈正相关。在这些菌株中测定了曲安奈德的腭裂剂量-反应曲线，但它们并不像可的松那样彼此平行。曲安奈德可能通过不同的机制引起腭裂。胎鼠组织含有明显的糖皮质激素受体，但其与小鼠腭裂形成的关系尚不清楚。
Fetal mouse tissue was investigated for a glucocorticoid binding receptor which might be responsible for cleft palate formation. Fetal mouse heads contain a soluble component which binds the glucocorticoid triamcinolone acetonide in vitro with high affinity. This binding component is present in small finite amounts. Other glucocorticoids compete with triamcinolone acetonide for the binding site in a manner consistent with their potency ranking as cleft palate teratogens. Several mineralocorticoids and progestins also compete when administered in vitro but not when administered in vivo. Triamcinolone acetonide binding was determined in 3 mouse strains, A/J, C3H and C57BL, which are listed in decreasing order of cleft palate susceptibility to cortisone. No positive correlation was found between cortisone cleft palate susceptibility and triamcinolone acetonide binding affinity or binding amount in fetuses from these strains. Cleft palate dose-response curves for triamcinolone acetonide were determined in these strains, but they were not parallel to each other as they were for cortisone. Triamcinolone acetonide may cause cleft palate by different mechanisms in these strains. Fetal mouse tissue contains an apparent glucocorticoid receptor, but its relationship to cleft palate formation in mice is not clear.