Hyperoxaluric rats do not exhibit alterations in renal expression patterns of Slc26a1 (SAT1) mRNA or protein.

Urological Research Pub Date : 2012-12-01 Epub Date: 2012-05-10 DOI:10.1007/s00240-012-0480-4
Robert W Freel, Marguerite Hatch
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引用次数: 6

Abstract

Little is known about oxalate transport in renal epithelia under basal conditions, let alone in hyperoxaluria when the capacity for renal oxalate excretion is increased. Sulfate anion transporter 1 (SAT1, Slc26a1) is considered to be a major basolateral anion-oxalate exchanger in the proximal tubule and we hypothesized its expression may correlate with urinary oxalate excretion. We quantified changes in the renal expression of SAT1 mRNA and protein in two rat models, one with hyperoxaluria (HYP) and one with renal insufficiency (HRF) induced by hyperoxaluria. The hyperoxaluria observed in the HYP group could not simply be ascribed to changes in SAT1 mRNA or protein abundance. However, when hyperoxaluria was accompanied by renal insufficiency, significant reductions in SAT1 mRNA and protein were detected in medullary and papillary tissue. Together, the results indicate that transcriptional modulation of the SAT1 gene is not a significant component of the hyperoxaluria observed in these rat models.

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高血氧大鼠的肾脏Slc26a1 (SAT1) mRNA或蛋白的表达模式没有改变。
在基础条件下,草酸盐在肾上皮中的转运知之甚少,更不用说当肾脏草酸盐排泄能力增加时的高草酸尿。硫酸盐阴离子转运蛋白1 (SAT1, Slc26a1)被认为是近端小管中主要的基底外侧阴离子-草酸盐交换体,我们假设其表达可能与尿草酸盐排泄有关。我们量化了高草酸尿(HYP)和高草酸尿引起的肾功能不全(HRF)两种大鼠模型中SAT1 mRNA和蛋白表达的变化。在HYP组中观察到的高草酸尿不能简单地归因于SAT1 mRNA或蛋白质丰度的变化。然而,当高草酸尿伴有肾功能不全时,髓质和乳头状组织中检测到SAT1 mRNA和蛋白的显著减少。综上所述,结果表明SAT1基因的转录调节并不是这些大鼠模型中观察到的高盐尿的重要组成部分。
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来源期刊
Urological Research
Urological Research 医学-泌尿学与肾脏学
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6-12 weeks
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