Solé E, Calvo R, Obregón M J, Meseguer A
Unitat de Recerca Biomédica, Hospital Materno-Infantil Vall d'Hebrón, Barcelona, Spain.
Mol Cell Endocrinol. 1996 May 31;119(2):147-59. doi: 10.1016/0303-7207(96)03603-9.
The kidney androgen-regulated protein (KAP) gene exhibits a cell-specific hormonal regulation of its expression in the epithelial cells of proximal tubules of mouse kidney, where T3 is required for constitutive expression in the straight segments and androgens for expression in the convoluted ones. By using different models of hypothyroidism, we demonstrate that maximal androgen-mediated induction of the gene depends on thyroid hormone as well. This constitutes a specific event, since vitamin D3 cannot mimic the effects of T3, albeit their remarkable functional relationship. It is also shown that while congenital hypothyroid hyt/hyt male mice, exposed to maternal T3 in the gestational period, exhibit diminished but existent androgen-dependent cortical responses, mice exposed to goitrogens during gestation and postnatally are unable to express the gene even at postnatal day ninety. Impairment of KAP cortical expression in hypothyroid animals does not correlate with lower levels of androgens or androgen receptor expression.
肾雄激素调节蛋白（KAP）基因在小鼠肾脏近端小管上皮细胞中呈现出细胞特异性的激素表达调控，其中在直段中组成性表达需要T3，而在曲段中表达需要雄激素。通过使用不同的甲状腺功能减退模型，我们证明该基因的最大雄激素介导诱导也依赖于甲状腺激素。这构成了一个特定事件，因为尽管维生素D3与T3有显著的功能关系，但它不能模拟T3的作用。还表明，虽然先天性甲状腺功能减退的hyt/hyt雄性小鼠在妊娠期暴露于母体T3时，雄激素依赖性皮质反应减弱但仍然存在，但在妊娠期和出生后暴露于致甲状腺肿物质的小鼠即使在出生后第90天也无法表达该基因。甲状腺功能减退动物中KAP皮质表达的受损与雄激素或雄激素受体表达水平降低无关。
