Biber J, Forgo J, Murer H
Institute of Physiology, University of Zurich, Switzerland.
Am J Physiol. 1988 Aug;255(2 Pt 1):C155-61. doi: 10.1152/ajpcell.1988.255.2.C155.
The effect of the extracellular concentration of Pi on the Na+-dependent phosphate transport activity of OK cells was investigated. When incubated with extracellular Pi at concentrations of 200 microM or less, Na+-Pi cotransport increased approximately twofold in OK cells compared with control cells (kept in 0.85 mM Pi), whereas other Na+-dependent transport activities were not affected. After Pi deprivation, Na+-Pi cotransport could be inhibited to a similar extent (80%) by parathyroid hormone (PTH) as in control cells, suggesting that the PTH-sensitive Na+-Pi cotransport activity is also regulated by extracellular Pi. The increase of Na+-Pi cotransport was maximally expressed after 6 h and could be prevented by cycloheximide (70 microM) but not by actinomycin D (0.5-5 g/ml). However, the adaptive response was completely blocked by 3'-deoxyadenosine (cordycepin) at 100 microM. From these data, it is concluded that the upregulation of Na+-Pi cotransport in OK cells due to low extracellular Pi is controlled at a posttranscriptional level.
研究了细胞外无机磷酸盐（Pi）浓度对OK细胞钠依赖型磷酸盐转运活性的影响。当与浓度为200微摩尔/升或更低的细胞外Pi孵育时，与对照细胞（置于0.85毫摩尔/升Pi中）相比，OK细胞中的钠-磷酸盐共转运增加了约两倍，而其他钠依赖型转运活性未受影响。在Pi缺乏后，甲状旁腺激素（PTH）对钠-磷酸盐共转运的抑制程度（80%）与对照细胞相似，这表明PTH敏感的钠-磷酸盐共转运活性也受细胞外Pi的调节。钠-磷酸盐共转运的增加在6小时后达到最大表达，并且可以被放线菌酮（70微摩尔）阻止，但不能被放线菌素D（0.5 - 5微克/毫升）阻止。然而，100微摩尔的3'-脱氧腺苷（虫草素）完全阻断了适应性反应。从这些数据可以得出结论，细胞外低Pi导致的OK细胞中钠-磷酸盐共转运上调是在转录后水平受到控制的。
