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UMR 106 成骨样细胞中磷酸盐(Pi)浓度的调节:Pi、Na⁺ 和 K⁺ 的作用

Regulation of the phosphate (Pi) concentration in UMR 106 osteoblast-like cells: effect of Pi, Na+ and K+.

作者信息

Kemp G J, Khouja H I, Ahmado A, Graham R, Russell G, Bevington A

机构信息

Department of Human Metabolism and Clinical Biochemistry, Medical School, Sheffield, U.K.

出版信息

Cell Biochem Funct. 1993 Mar;11(1):13-23. doi: 10.1002/cbf.290110103.

Abstract

Osteoblast-like cells possess Na-dependent transporters which accumulate orthophosphate (Pi) from the extracellular medium. This may be important in bone formation. Here we describe parallel measurements of Pi uptake and cellular [Pi] in such cells from the rat (UMR 106-01 and UMR 106-06) and human (OB), and in non-osteoblastic human fibroblasts (Detroit 532 (DET)). In UMR 106-01, cellular [Pi] was weakly dependent on extracellular [Pi] and higher than expected from passive transport alone. [32Pi]-uptake was inhibited by Na deprivation, but paradoxically increased on K deprivation. With Na, 87 per cent of cellular 32P was found in organic phosphorus pools after only 5 min. Na deprivation also decreased cellular [Pi], in both UMR 106-01 and DET, but the decrease was smaller than that in [32Pi]-uptake. Ouabain decreased [32Pi]-uptake and cellular [Pi] in DET, but not in UMR 106-01. Regulation of cellular [Pi] is therefore at least partly dependent on Na/Pi co-transport, but this does not seem to be an exclusive property of osteoblasts.

摘要

成骨样细胞具有钠依赖性转运体,可从细胞外介质中积累正磷酸盐(Pi)。这在骨形成中可能很重要。在此,我们描述了对大鼠(UMR 106 - 01和UMR 106 - 06)和人类(OB)的此类细胞以及非成骨人类成纤维细胞(底特律532(DET))中Pi摄取和细胞内[Pi]的平行测量。在UMR 106 - 01中,细胞内[Pi]对细胞外[Pi]的依赖性较弱,且高于仅通过被动转运所预期的值。[32P] - 摄取受到钠缺乏的抑制,但矛盾的是,在钾缺乏时增加。有钠存在时,仅5分钟后87%的细胞内32P就存在于有机磷池中。钠缺乏也会降低UMR 106 - 01和DET中的细胞内[Pi],但降低幅度小于[32P] - 摄取的降低幅度。哇巴因降低了DET中的[32P] - 摄取和细胞内[Pi],但对UMR 106 - 01没有影响。因此,细胞内[Pi]的调节至少部分依赖于钠/磷共转运,但这似乎并非成骨细胞所特有的特性。

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