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首页> 外文期刊>American Journal of Physiology >Differential effects of Npt2a gene ablation and X-linked Hyp mutation on renal expression of Npt2c.
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Differential effects of Npt2a gene ablation and X-linked Hyp mutation on renal expression of Npt2c.

机译：Npt2a基因切除和X连锁Hyp突变对Npt2c肾脏表达的差异作用。

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摘要

The present study was undertaken to define the mechanisms governing the regulation of the novel renal brush-border membrane (BBM) Na-phosphate (Pi) cotransporter designated type IIc (Npt2c). To address this issue, the renal expression of Npt2c was compared in two hypophosphatemic mouse models with impaired renal BBM Na-Pi cotransport. In mice homozygous for the disrupted Npt2a gene (Npt2-/-), BBM Npt2c protein abundance, relative to actin, was increased 2.8-fold compared with Npt2+/+ littermates, whereas a corresponding increase in renal Npt2c mRNA abundance, relative to beta-actin, was not evident. In contrast, in X-linked Hyp mice, which harbor a large deletion in the Phex gene, the renal abundance of both Npt2c protein and mRNA was significantly decreased by 80 and 50%, respectively, relative to normal littermates. Pi deprivation elicited a 2.5-fold increase in BBM Npt2c protein abundance in Npt2+/+ mice but failed to elicit a further increase in Npt2c protein in Npt2-/- mice. Pi restriction led to an increase in BBM Npt2c protein abundance in both normal and Hyp mice without correcting its renal expression in the mutants. In summary, we report that BBM Npt2c protein expression is differentially regulated in Npt2-/- mice and Hyp mice and that the Npt2c response to low-Pi challenge differs in both hypophosphatemic mouse strains. We demonstrate that Npt2c protein is maximally upregulated in Npt2-/- mice and suggest that Npt2c likely accounts for residual BBM Na-Pi cotransport in the knockout model. Finally, our data indicate that loss of Phex function abrogates renal Npt2c protein expression.
机译：进行本研究以定义控制新型IIc（Npt2c）型肾刷状边界膜（BBM）磷酸钠（Pi）共转运蛋白的调控机制。为了解决这个问题，在肾血BBM Na-Pi共转运受损的两个低磷酸盐血症小鼠模型中比较了Npt2c的肾脏表达。与Npt2 + / +同窝仔猪相比，在Npt2a基因纯合子（Npt2-/-）纯合小鼠中，BBM Npt2c蛋白相对于肌动蛋白的含量增加了2.8倍，而肾脏Npt2c mRNA相对于β-肌动蛋白，并不明显。相比之下，在X链接的Hyp小鼠中，Phex基因存在大量缺失，相对于正常同窝仔，Npt2c蛋白和mRNA的肾脏丰度分别显着降低了80％和50％。 Pi剥夺导致Npt2 + / +小鼠中BBM Npt2c蛋白丰度增加2.5倍，但未能引起Npt2-/-小鼠Npt2c蛋白进一步增加。 Pi限制导致正常和Hyp小鼠的BBM Npt2c蛋白丰度增加，而没有纠正突变体中其肾脏的表达。总之，我们报告了BBM Npt2c蛋白表达在Npt2-/-小鼠和Hyp小鼠中受到差异调节，并且在低磷小鼠品系中，对低Pi挑战的Npt2c反应均不同。我们证明，Npt2c蛋白在Npt2-/-小鼠中最大上调，并暗示Npt2c可能解释了基因敲除模型中残留的BBM Na-Pi共转运。最后，我们的数据表明Phex功能丧失可消除肾脏Npt2c蛋白表达。

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