1,25-Dihydroxyvitamin D-stimulated calmodulin binding proteins: a sustained effect on distal tubules.

1,25-Dihydroxyvitamin D-stimulated calmodulin binding proteins: a sustained effect on distal tubules.
复制标题

1,25-二羟基维生素 D 刺激的钙调蛋白结合蛋白:对远端小管的持续影响。

DOI:
10.1152/ajprenal.00286.2000
复制
发表时间:
2002
期刊:
American journal of physiology. Renal physiology
影响因子:
--
通讯作者:
Walters,MarianR
Walters,MarianR
中科院分区:
--
文献类型:
--
作者:
Siaw,EmmanuelKO;Walters,MarianR

文献摘要

被引文献

相似文献

为了更好地了解体内长期1,25(OH)2D 3处理对大鼠肾脏的反应,对1,25-二羟维生素D[1,25(OH)2D 3]刺激的钙调素结合蛋白(CaMBP-Ds)在大鼠肾脏中的肾小管定位及其诱导的特异性进行了表征。没有其他激素(甲状旁腺激素、降钙素、雌二醇-17 β、睾酮、孕酮、氢化可的松或地塞米松)刺激CaMBP-Ds,而最大的1,25(OH)2D 3刺激发生在100 ng/天1,25(OH)2D 3治疗5- 7天后。除了更普遍分布的CaMBP-D150外,CaMBP-Ds定位于远端而非近端小管制剂。1,25(OH)2D 3对维生素D受体和CaMBP-Ds的诱导作用在剂量反应和时间过程方面相似。停药后CaMBP-Ds仍升高至少4周。由于维生素D刺激的肾脏CaMBP-Ds主要是远端小管的蛋白质,它们可能与肾脏调节Ca 2+稳态有关。CaMBP-Ds的持续诱导在解决其诱导是否是正常Ca 2+稳态的函数或高维生素D症和高钙血症的病理生理后果的问题中是重要的。
The tubular localization of 1,25-dihydroxyvitamin D[1,25(OH)2D3]-stimulated calmodulin binding proteins (CaMBP-Ds) in the rat kidney and the specificity of their induction were characterized to better understand renal responses to protracted 1,25(OH)2D3treatment in vivo. None of the other hormones tested (parathyroid hormone, calcitonin, estradiol-17β, testosterone, progesterone, hydrocortisone, or dexamethasone) stimulated the CaMBP-Ds, whereas maximal 1,25(OH)2D3stimulation occurred after a 5- to 7-day treatment with 100 ng/day 1,25(OH)2D3. With the exception of the more ubiquitously distributed CaMBP-D150, the CaMBP-Ds were localized in distal, but not proximal, tubule preparations. 1,25(OH)2D3induction of vitamin D receptors and the CaMBP-Ds was similar with respect to dose-response and time course. Finally, the CaMBP-Ds remained elevated for at least 4 wk after 1,25(OH)2D3withdrawal. Because the vitamin D-stimulated renal CaMBP-Ds are principally proteins of the distal tubule, they may be associated with renal regulation of Ca2+homeostasis. The sustained induction of CaMBP-Ds is important in addressing the question of whether their induction is a function of normal Ca2+homeostasis or a pathophysiological consequence of hypervitaminosis D and hypercalcemia.