Inoue T, Kawashima H
Department of Pharmacology, Jichi Medical School, Tochigi-ken, Japan.
Biochem Biophys Res Commun. 1988 May 16;152(3):1388-94. doi: 10.1016/s0006-291x(88)80439-x.
We have recently shown the presence of receptors for 1,25-dihydroxyvitamin D3 and that 1,25-dihydroxyvitamin D3 stimulates Ca-ATPase in vascular smooth muscle cells presumably via receptor mediated mechanism. These data suggest that the sterol may directly be involved in the regulation of cellular calcium homeostasis. To further define action of vitamin D in smooth muscle cells, we studied effect of the sterol on cellular uptake of calcium. 1,25-dihydroxyvitamin D3 stimulated 45Ca2+ uptake by cultured cells, A7r5, derived from fetal rat aorta, when the cells were incubated with the sterol for 18 hr. The effect was dose-dependent at 10(-10) to 10(-9) M, and three orders of magnitude higher concentration of 25-hydroxyvitamin D3 or 24,25-dihydroxyvitamin D3 was needed to obtain similar effects. Furthermore, the effect of 1,25-dihydroxyvitamin D3 was abolished by cycloheximide (10(-5) M), a protein synthesis inhibitor. These data clearly suggest that 1,25-dihydroxyvitamin D3 may directly regulate cellular calcium homeostasis in vascular smooth muscle cells presumably via receptor mediated mechanism.
我们最近发现了1,25 - 二羟基维生素D3的受体,并且1,25 - 二羟基维生素D3可能通过受体介导的机制刺激血管平滑肌细胞中的钙 - ATP酶。这些数据表明,这种甾醇可能直接参与细胞钙稳态的调节。为了进一步明确维生素D在平滑肌细胞中的作用,我们研究了这种甾醇对细胞钙摄取的影响。当将培养的源自胎鼠主动脉的A7r5细胞与这种甾醇孵育18小时时,1,25 - 二羟基维生素D3刺激了45Ca2+的摄取。在10(-10)至10(-9)M浓度范围内,这种作用呈剂量依赖性,并且需要比其高三个数量级浓度的25 - 羟基维生素D3或24,25 - 二羟基维生素D3才能获得类似的效果。此外,蛋白质合成抑制剂环己酰亚胺(10(-5)M)消除了1,25 - 二羟基维生素D3的作用。这些数据清楚地表明,1,25 - 二羟基维生素D3可能通过受体介导的机制直接调节血管平滑肌细胞中的细胞钙稳态。