胰岛素样生长因子I对培养近端小管细胞中磷酸盐转运的影响。

R Hirschberg, H Ding, C Wanner
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摘要

在体内,近端小管细胞暴露于存在于血清或近端小管液中的胰岛素样生长因子I (IGF-I)。例如,在肾病综合征中,近端小管液含有igf - 1,其浓度与igf结合蛋白-2 (IGFBP-2)相关,具有生物学意义。igf - 1也被证明可以减少正常受试者尿液中磷酸盐(Pi)的排泄。我们假设igf - 1可以通过顶端和底外侧小管受体机制直接提高小管细胞对Pi的吸收,特别是通过igf - 1 (I型)受体,而不是igf - 2 (II型)或胰岛素受体。研究在培养的表达高亲和力IGF-I受体的近端小管细胞中进行。用IGF-I(10(-9)至10(-7)mol/L)选择性地刺激细胞的顶端或基底外侧膜,可使Pi吸收增加80%,但在顶端到基底外侧方向上没有明显的反向Pi通量。igf - 1对Pi转运的影响似乎是特异性的,因为丙氨酸的转运不受肽的影响。IGFBP-2不抑制IGF-I的这种作用,但IGF-I诱导的Pi转运增加被中和性抗IGF-I受体单克隆抗体抑制。细胞暴露于IGF-II (10(-7) mol/L)而不是在顶膜处选择性暴露于胰岛素,倾向于增加Pi的运输,这种IGF-II的作用也被抗igf - i受体抗体阻断。(摘要删节250字)
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Effects of insulin-like growth factor I on phosphate transport in cultured proximal tubule cells.

In vivo, proximal tubule cells are exposed to insulin-like growth factor I (IGF-I) that is present in serum or in proximal tubule fluid. For example, in the nephrotic syndrome, proximal tubule fluid contains IGF-I at biologically meaningful concentrations in association with IGF-binding protein-2 (IGFBP-2). IGF-I has also been shown to decrease the urinary excretion of phosphate (Pi) in normal subjects. We hypothesized that IGF-I can raise tubule cell Pi absorption directly through an apical as well as a basolateral tubule receptor mechanism, specifically, through IGF-I (type I) receptors as compared to IGF-II (type II) or insulin receptors. Studies were performed in cultured proximal tubule cells that express high-affinity IGF-I receptors. Stimulation of cells selectively at the apical or basolateral membrane with IGF-I (10(-9) to 10(-7) mol/L) increases Pi absorption by up to 80%, but a significant counterdirectional Pi flux in the apical-to-basolateral direction does not occur. The effect of IGF-I on Pi transport appears to be specific inasmuch as the transport of alanine is not affected by the peptide. IGFBP-2 does not inhibit this effect of IGF-I, but the IGF-I-induced increase in Pi transport is inhibited by a neutralizing anti-IGF-I receptor monoclonal antibody. Exposure of the cells to IGF-II (10(-7) mol/L) but not to insulin selectively at the apical membrane tends to increase Pi transport, and this IGF-II effect is also blocked by the anti-IGF-I receptor antibody.(ABSTRACT TRUNCATED AT 250 WORDS)

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