Role of pendrin in iodide balance: going with the flow
Role of pendrin in iodide balance: going with the flow
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DOI：
10.1152/ajprenal.90581.2008
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发表时间：
2009-10-01
影响因子：
4.2
通讯作者：
Wall, Susan M.
中科院分区：
文献类型：
--
作者：
Kim, Young Hee;Pham, Truyen D.;Wall, Susan M.
Kim YH，Pham TD，Zheng W，Hong S，Baylis C，Pech V，Beierwaltes WH，法利DB，Braverman LE，Verlander JW，Wall SM. pendrin在碘平衡中的作用：顺其自然。美国肾脏生理学杂志297：F1069-F1079，2009年。首次发表于2009年7月15日; doi：10.1152/ajprenal.90581.2008。Pendrin在B型和非A型、非B型闰间细胞的顶端区域中表达，在那里它通过顶端Cl-/HCO 3-交换介导Cl-吸收和HCO 3-分泌。由于pendrin是一种强有力的I-转运蛋白，我们询问pendrin是否在饮食I-限制下上调，以及它是否调节I-平衡.因此，在pendrin无效和野生型小鼠中测定I-平衡。Pendrin丰度进行了评估，免疫印迹，免疫组化和免疫金细胞化学与形态分析。虽然pendrin丰度不变时，饮食中的I-摄入量在生理范围内变化，I-平衡不同pendrin空和野生型小鼠。血清I-较低，而I-排泄较高pendrin空相对于野生型小鼠，与肾脏I-吸收的作用pendrin一致。增加H2O摄入增强了野生型和pendrin缺失小鼠之间I-平衡的差异，表明H2O摄入调节pendrin丰度。将饮水量从接近4 ml/天提高到接近11 ml/天，B细胞顶端质膜与细胞质pendrin标记的比率增加了75%，尽管循环中的肾素、醛固酮和血清渗透压没有变化。进一步的研究询问H2O摄入是否通过AVP的作用调节pendrin。我们观察到，H2O摄入调制pendrin丰度，即使循环加压素水平被钳制。我们的结论是，水的摄入量调节pendrin丰度，虽然不太可能通过直接的，2型加压素受体依赖性机制。随着水摄入量的增加，pendrin在维持Cl-和I-平衡方面变得越来越重要。
Kim YH, Pham TD, Zheng W, Hong S, Baylis C, Pech V, Beierwaltes WH, Farley DB, Braverman LE, Verlander JW, Wall SM. Role of pendrin in iodide balance: going with the flow. Am J Physiol Renal Physiol 297: F1069-F1079, 2009. First published July 15, 2009; doi:10.1152/ajprenal.90581.2008.-Pendrin is expressed in the apical regions of type B and non-A, non-B intercalated cells, where it mediates Cl- absorption and HCO3- secretion through apical Cl-/HCO3- exchange. Since pendrin is a robust I- transporter, we asked whether pendrin is upregulated with dietary I- restriction and whether it modulates I- balance. Thus I- balance was determined in pendrin null and in wild-type mice. Pendrin abundance was evaluated with immunoblots, immunohistochemistry, and immunogold cytochemistry with morphometric analysis. While pendrin abundance was unchanged when dietary I- intake was varied over the physiological range, I- balance differed in pendrin null and in wild-type mice. Serum I- was lower, while I- excretion was higher in pendrin null relative to wild-type mice, consistent with a role of pendrin in renal I- absorption. Increased H2O intake enhanced differences between wild-type and pendrin null mice in I- balance, suggesting that H2O intake modulates pendrin abundance. Raising water intake from similar to 4 to similar to 11 ml/day increased the ratio of B cell apical plasma membrane to cytoplasm pendrin label by 75%, although circulating renin, aldosterone, and serum osmolality were unchanged. Further studies asked whether H2O intake modulates pendrin through the action of AVP. We observed that H2O intake modulated pendrin abundance even when circulating vasopressin levels were clamped. We conclude that H2O intake modulates pendrin abundance, although not likely through a direct, type 2 vasopressin receptor-dependent mechanism. As water intake rises, pendrin becomes increasingly critical in the maintenance of Cl- and I- balance.