Induction of hypertrophy in cultured proximal tubule cells by extracellular NH4Cl.
Induction of hypertrophy in cultured proximal tubule cells by extracellular NH4Cl.
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细胞外 NH4Cl 诱导培养的近端小管细胞肥大。
DOI：
10.1172/jci114361
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发表时间：
1989
期刊：
影响因子：
--
通讯作者：
Kurtz,I
中科院分区：
文献类型：
--
作者：
Golchini,K;Norman,J;Bohman,R;Kurtz,I
在体内，几种肾脏肥大模型的氨产量增加。本研究旨在确定在细胞外酸度没有变化的情况下，氨是否可以直接调节肾细胞的生长。在无血清介质中，NH4Cl(0-20 mM)以剂量依赖方式诱导JTC细胞和原代培养的兔近端小管细胞肥大(细胞蛋白质含量增加)，但不改变DNA合成。对JTC细胞的研究表明，由于蛋白质合成增加和蛋白质降解减少，细胞蛋白质含量增加。NH4Cl暴露后，细胞总RNA含量和核糖体数量增加，溶酶体酶组织蛋白酶B和L的细胞含量下降。用阿米洛利抑制Na+/H+逆向转运体并不能阻止NH4Cl诱导的肥大反应。结果表明，氨是肾细胞生长的重要调节因子，在缺乏功能性Na+/H+反转运活性的情况下，可能会发生肥大。
Ammonia production increases in several models of renal hypertrophy in vivo. The present study was designed to determine whether ammonia can directly modulate the growth of renal cells in the absence of a change in extracellular acidity. In serum-free media NH4Cl (0-20 mM) caused JTC cells and a primary culture of rabbit proximal tubule cells to hypertrophy (increase in cell protein content) in a dose-dependent fashion without a change in DNA synthesis. Studies in JTC cells revealed that the cell protein content increased as a result of both an increase in protein synthesis and a decrease in protein degradation. Total cell RNA content and ribosome number increased after NH4Cl exposure and the cell content of the lysosomal enzymes cathepsin B and L decreased. Inhibition of the Na+/H+ antiporter with amiloride did not prevent the hypertrophic response induced by NH4Cl. The results indicate that ammonia is an important modulator of renal cell growth and that hypertrophy can occur in the absence of functioning Na+/H+ antiport activity.Images