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首页> 外文期刊>American Journal of Physiology >Increased expression but not targeting of ENaC in adrenalectomized rats with PAN-induced nephrotic syndrome.
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Increased expression but not targeting of ENaC in adrenalectomized rats with PAN-induced nephrotic syndrome.

机译：在肾上腺切除的PAN引起的肾病综合征中，表达增加但不靶向ENaC。

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Sodium retention is a hallmark of nephrotic syndrome (NS). Puromycin aminonucleoside (PAN)-induced NS is associated with high aldosterone levels and increased ENaC expression and apical targeting. However, the mechanisms associated with increased apical targeting of ENaC in NS remain undefined, and it is unclear whether this is secondary to high aldosterone levels and whether aldosterone and/or apical ENaC targeting are important for the development of sodium retention. This study aimed at uncovering 1) whether aldosterone is essential for sodium retention in PAN-induced NS, 2) whether ENaC expression or apical targeting is secondary to high aldosterone levels, and 3) the role of aldosterone in the dysregulation of sodium transporters in NS. Puromycin treatment of adrenalectomized (ADX) rats supplemented with dexamethasone induced sodium retention despite the absence of aldosterone. Immunocytochemical analyses revealed an absence of enhanced apical targeting of ENaC subunits in PAN-treated ADX (ADX-PAN) rats, with distribution of labeling similar to adrenalectomized dexamethasone-treated control rats (ADX). Moreover, ENaC subunit abundance was increased in ADX-PAN rats. The abundance of aquaporin-2 was unchanged, whereas apical targeting was enhanced. Key sodium transporters were downregulated as previously observed in nonadrenalectomized puromycin-treated rats (Kim SW, Wang W, Nielsen J, Praetorius J, Kwon TH, Knepper MA, Frokiaer J, and Nielsen S. Am J Physiol Renal Physiol 286: F922-F935, 2004), whereas the global expression of the alpha1-subunit of the Na-K-ATPase was unchanged. In conclusion, PAN treatment in the absence of aldosterone induced sodium retention, increased ENaC expression, but did not change the subcellular distribution of ENaC. This indicates that the previously observed enhanced apical targeting of ENaC in PAN-induced NS (Kim SW, Wang W, Nielsen J, Praetorius J, Kwon TH, Knepper MA, Frokiaer J, and Nielsen S. Am J Physiol Renal Physiol 286: F922-F935, 2004) is caused by aldosterone and that development of sodium retention can occur in the absence of aldosterone in NS.
机译：钠retention留是肾病综合征（NS）的标志。嘌呤霉素氨基核苷（PAN）诱导的NS与醛固酮水平高，ENaC表达增加和根尖靶向有关。然而，与NS中ENaC的根尖靶向增加相关的机制仍然不确定，并且尚不清楚这是否是高醛固酮水平的继发者以及醛固酮和/或根尖ENaC靶向对于钠retention留的发展是否重要。这项研究旨在揭示1）醛固酮对于PAN诱导的NS中的钠retention留是否必不可少; 2）ENaC表达或根尖定位是否是高醛固酮水平的继发因素; 3）醛固酮在NS钠转运蛋白失调中的作用。 。尽管没有醛固酮，但嘌呤霉素治疗的肾上腺切除（ADX）大鼠补充地塞米松仍能引起钠retention留。免疫细胞化学分析显示，在PAN治疗的ADX（ADX-PAN）大鼠中，ENaC亚基的根尖定位不增强，其标记分布类似于经肾上腺切除的地塞米松治疗的对照大鼠（ADX）。此外，在ADX-PAN大鼠中，ENaC亚基的丰度增加。水通道蛋白2的丰度保持不变，而根尖靶向增强。如先前在未经肾上腺切除术的嘌呤霉素治疗的大鼠中观察到的那样，关键的钠转运蛋白被下调（Kim SW，Wang W，Nielsen J，Praetorius J，Kwon TH，Knepper MA，Frokiaer J和Nielsen S. Am J Physiol Renal Physiol 286：F922-F935 ，2004），而Na-K-ATPaseα1亚基的整体表达没有变化。总之，在没有醛固酮的情况下进行PAN处理可导致钠retention留，增加ENaC的表达，但不会改变ENaC的亚细胞分布。这表明先前观察到的PAN诱导的NS中ENaC的根尖靶向增强（Kim SW，Wang W，Nielsen J，Praetorius J，Kwon TH，Knepper MA，Frokiaer J和Nielsen S.Am J Physiol Renal Physiol 286：F922 -F935，2004）是由醛固酮引起的，并且在NS中不存在醛固酮的情况下会发生钠retention留。

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