Chandler J S, Chandler S K, Pike J W, Haussler M R
J Biol Chem. 1984 Feb 25;259(4):2214-22.
A consequence of 1,25-dihydroxyvitamin D3 (1,25-(OH)2D3) action in kidney is the enhanced production of 24,25-dihydroxyvitamin D3 (24,25-(OH)2D3). We have studied this apparent induction phenomenon in two established mammalian cell lines of renal origin. A porcine kidney cell line, LLC-PK1, was found to possess typical receptors for 1,25-(OH)2D3 which sediment at 3.3 S and bind to immobilized DNA. Saturation analysis of LLC-PK1 cell cytosol revealed an equilibrium binding constant (Kd) for 1,25-(OH)2D3 of 7.8 X 10(-11) M and a concentration of 5400 binding sites/cell. In the presence of serum, intact LLC-PK1 cells also internalize and bind 1,25-(OH)2D3. In contrast, a monkey kidney cell line, LLC-MK2, was found to contain a negligible concentration of the 1,25-(OH)2D3 receptor by all criteria examined. However, both renal cell lines respond to 1,25-(OH)2D3 with a 2- to 20-fold increase in basal levels of 25-hydroxyvitamin D3-24-hydroxylase (24-hydroxylase) activity. Incubation of viable cell suspensions with 25-hydroxy[26,27-3H]vitamin D3 (0.5 microM) at 37 degrees C for 30 min followed by subsequent analysis of lipid extracts via high performance liquid chromatography was carried out to assess 24,25-(OH)2[3H]D3 formation. Enzyme induction was found to be specific for 1,25-(OH)2D3 in both cell lines with half-maximal stimulation of 24-hydroxylase activity observed at 0.2 and greater than or equal to 1.0 nM 1,25-(OH)2D3 in LLC-PK1 and LLC-MK2, respectively. The response in LLC-PK1 was more rapid (1-4 h) than in LLC-MK2 (4-8 h) following 1,25-(OH)2D3 treatment of cultures in situ. In both cell lines, actinomycin D abolished the 1,25-(OH)2D3-dependent increase in 24-hydroxylase activity. Our results suggest that the high affinity 1,25-(OH)2D3 receptor may not be required for 1,25-(OH)2D3-dependent induction of renal 24-hydroxylase activity. Alternatively, LLC-MK2 cells could contain an atypical form of the 1,25-(OH)2D3 receptor protein which retains functionality but escapes detection by standard binding techniques.
1,25 - 二羟基维生素D3(1,25 - (OH)2D3)在肾脏中作用的一个结果是24,25 - 二羟基维生素D3(24,25 - (OH)2D3)生成增加。我们在两种已建立的源自肾脏的哺乳动物细胞系中研究了这种明显的诱导现象。发现一种猪肾细胞系LLC - PK1具有典型的1,25 - (OH)2D3受体,该受体在3.3 S沉降并与固定化DNA结合。对LLC - PK1细胞胞质溶胶的饱和分析显示,1,25 - (OH)2D3的平衡结合常数(Kd)为7.8×10(-11) M,每个细胞有5400个结合位点。在有血清存在的情况下,完整的LLC - PK1细胞也会内化并结合1,25 - (OH)2D3。相比之下,通过所有检测标准发现一种猴肾细胞系LLC - MK2中1,25 - (OH)2D3受体的浓度可忽略不计。然而,两种肾细胞系对1,25 - (OH)2D3的反应都是使25 - 羟基维生素D3 - 24 - 羟化酶(24 - 羟化酶)活性的基础水平增加2至20倍。将活细胞悬液与25 - 羟基[26,27 - 3H]维生素D3(0.5 microM)在37℃孵育30分钟,随后通过高效液相色谱对脂质提取物进行后续分析,以评估24,25 - (OH)2[3H]D3的形成。发现在两种细胞系中,酶诱导对1,25 - (OH)2D3具有特异性,在LLC - PK1和LLC - MK2中,分别在0.2 nM和大于或等于1.0 nM的1,25 - (OH)2D3时观察到24 - 羟化酶活性的半最大刺激。在原位用1,25 - (OH)2D3处理培养物后,LLC - PK1中的反应比LLC - MK2(4 - 8小时)更快(1 - 4小时)。在两种细胞系中,放线菌素D都消除了1,25 - (OH)2D3依赖性的24 - 羟化酶活性增加。我们的结果表明,1,25 - (OH)2D3依赖性诱导肾24 - 羟化酶活性可能不需要高亲和力的1,25 - (OH)2D3受体。或者,LLC - MK2细胞可能含有1,25 - (OH)2D3受体蛋白的一种非典型形式,该形式保留功能但通过标准结合技术无法检测到。