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首页> 外文期刊>Journal of Epithelial Biology & Pharmacology >Regulation of Renal LAT2 and 4F2hc Expression by Aldosterone
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Regulation of Renal LAT2 and 4F2hc Expression by Aldosterone

机译：醛固酮对肾脏LAT2和4F2hc表达的调节

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In the spontaneous hypertensive rat, overexpression of the renal Na+-independent L-amino acid transporterLAT2 is organ specific, precedes the onset of hypertension, correlates negatively with plasma aldosterone, and parallelsthe enhanced ability to take up L-DOPA and form renal dopamine. The present study evaluated the role of aldosterone ontranscript and protein abundance of Na+-independent and Na+-dependent amino acid transporters. Na+-independent heterodimericamino acid transporters LAT1/4F2hc, LAT2/4F2hc and a Na+-dependent transporter ASCT2 transcript andprotein abundance was determined in the renal cortex of normotensive Wistar rats chronically treated with aldosterone(1.5 mg), spironolactone (200 mg) or aldosterone plus spironolactone. Aldosterone significantly increased renal corticalLAT2 mRNA levels (45 % increase), with no changes in LAT1, 4F2hc and ASCT2 transcript levels. The effect of aldosteroneupon LAT2 mRNA levels was completely prevented by spironolactone. At the protein level, aldosterone treatmentdid not significantly affect LAT1 and LAT2 expression, but markedly reduced (51 % decrease) the abundance of 4F2hcand the urinary excretion of dopamine and DOPAC. The effect of aldosterone upon 4F2hc protein abundance was not reversedby spironolactone. Increases in renal LAT2 transcript during chronic treatment with aldosterone occur through aspironolactone-sensitive genomic mechanism. This effect parallels with a decrease in LAT2 functionality, resulting fromdecreases in 4F2hc protein abundance, which appears to be either a non-genomic effect or an indirect effect of aldosterone.The decrease in LAT2 functionality by aldosterone correlates well with the reduction in urinary dopamine.
机译：在自发性高血压大鼠中，肾脏Na +依赖性L-氨基酸转运蛋白LAT2的过度表达是器官特异性的，在高血压发作之前，与血浆醛固酮呈负相关，并且与增强的摄取L-DOPA和形成肾脏多巴胺的能力平行。本研究评估了醛固酮转录物的作用以及不依赖Na +和依赖Na +的氨基酸转运蛋白的蛋白质丰度。在经醛固酮（1.5 mg），螺内酯（200 mg）或醛固酮加醛固酮长期治疗的正常血压Wistar大鼠的肾皮质中，测定了Na +依赖性异二聚氨基酸转运蛋白LAT1 / 4F2hc，LAT2 / 4F2hc和Na +依赖性转运蛋白ASCT2转录和蛋白质丰度。螺内酯。醛固酮显着增加肾皮质LAT2 mRNA水平（增加45％），而LAT1、4F2hc和ASCT2转录水平无变化。螺内酯完全阻止了醛固酮对LAT2 mRNA水平的影响。在蛋白质水平上，醛固酮处理不会显着影响LAT1和LAT2的表达，但显着降低（降低了51％）4F2的丰度，可以阻止多巴胺和DOPAC的尿排泄。螺内酯不能逆转醛固酮对4F2hc蛋白丰度的影响。通过对阿司匹林内酯敏感的基因组机制，在醛固酮长期治疗过程中肾脏LAT2转录水平的增加。这种作用与由于4F2hc蛋白丰度降低而导致的LAT2功能降低同时出现，这似乎是醛固酮的非基因组效应或间接作用。醛固酮导致LAT2功能的降低与尿液多巴胺的降低密切相关。

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