Renal growth hormone--insulin-like growth factor-I system in acute renal failure.
Renal growth hormone--insulin-like growth factor-I system in acute renal failure.
复制标题
肾生长激素——胰岛素样生长因子-I系统在急性肾功能衰竭中的作用。
DOI：
10.1038/ki.1995.230
复制
发表时间：
1995
影响因子：
19.6
通讯作者：
Rabkin,R
中科院分区：
文献类型：
--
作者：
Tsao,T;Wang,J;Fervenza,FC;Vu,TH;Jin,IH;Hoffman,AR;Rabkin,R
肾生长激素-胰岛素样生长因子- 1系统在急性肾衰竭中的作用。肾生长激素-胰岛素样生长因子- 1系统在急性缺血性肾衰竭中的作用。IGF-I治疗可加速急性肾小管坏死（ATN）的恢复。此外，局部肾生长激素- igf - i系统可能参与自然修复。我们检测了60分钟缺血大鼠肾脏中的IGF-I系统，并与假手术对照进行了比较。损伤后2天，生长激素受体mRNA和IGF-I mRNA水平下降了控制值的9% ~ 33%。这与肾脏免疫反应性IGF-I水平降低有关。相比之下，igf - 1受体mRNA丰度没有变化。然而，第2天和第7天的质膜IGF-I受体结合量几乎是对照组的两倍（P < 0.01）。Scatchard分析显示，受体数量增加了近两倍。由于受体mRNA水平不变，这意味着受体蛋白上调。与IGF-I受体mRNA水平不变相比，损伤后第2天，胰岛素样生长因子结合蛋白(IGFBP) -2、-3、-4和-5的mRNA丰度下降了约14%至62% (P < 0.05)，表明IGFBP的产生减少。因此，肾对缺血性ATN的反应，即低IGFBP mRNA水平和高IGF-I受体数量，可能会增加IGF-I的生物利用度，从而增强局部和循环IGF-I在缺血性ATN中的修复作用。
Renal growth hormone—insulin-like growth factor-I system in acute renal failure. The renal growth hormone—insulin-like growth factor-I system in acute ischemic renal failure. Recovery from acute tubular necrosis (ATN) is accelerated by IGF-I therapy. Furthermore, the local renal growth hormone-IGF-I system may participate in the natural repair. We examined the IGF-I system in rat kidneys subjected to 60 minute ischemia compared to sham operated controls. Two days after injury, growth hormone receptor mRNA and IGF-I mRNA levels fell ∼9 to 33% of control values. This was associated with a reduction in kidney immunoreactive IGF-I levels. In contrast, IGF-I receptor mRNA abundance was unchanged. However, plasma membrane IGF-I receptor binding on day 2 and day 7 was near double the control values (P < 0.01). Scatchard analysis revealed a near twofold increase in receptor number. Since receptor mRNA levels were unchanged, this implies receptor protein up-regulation. In contrast to unchanged IGF-I receptor mRNA levels, the abundance of mRNA levels of insulin-like growth factor binding proteins (IGFBP) -2, -3, -4 and -5 fell ∼14 to 62% of control levels day 2 after injury (P < 0.05), suggesting reduced IGFBP production. Thus, the renal response to ischemic ATN, namely, low IGFBP mRNA levels and high IGF-I receptor number, may function to increase IGF-I bioavailability and thereby enhance the reparative actions of local and circulating IGF-I in ischemic ATN.