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Sequential expression of NKCC2, TonEBP, aldose reductase, and urea transporter-A in developing mouse kidney.

Sequential expression of NKCC2, TonEBP, aldose reductase, and urea transporter-A in developing mouse kidney. Research Abstract Details 

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  • Sequential expression of NKCC2, TonEBP, aldose reductase, and urea transporter-A in developing mouse kidney. Abstract Text:

    hyun-wook leeHyun-Wook Lee,wan-young kimWan-Young Kim,hyun-kuk songHyun-Kuk Song,chul-woo yangChul-Woo Yang,ki-hwan hanKi-Hwan Han,h moo kwonH Moo Kwon,jin kimJin Kim,

    This study was conducted to test the hypothesis that, during renal development, the Na-K-2Cl cotransporter type 2 (NKCC2) activates the tonicity-responsive enhancer binding protein (TonEBP) transcription factor by creating medullary hypertonicity. TonEBP, in turn, drives the expression of aldose reductase (AR) and urea transporter-A (UT-A). Kidneys from 13- to19-day-old fetuses (F13-F19), 1- to 21-day-old pups (P1-P21), and adult mice were examined by immunohistochemistry. NKCC2 was first detected on F14 in differentiating macula densa and thick ascending limb (TAL). TonEBP was first detected on F15 in the medullary collecting duct (MCD) and surrounding endothelial cells. AR was detected in the MCD cells of the renal medulla from F15. UT-A first appeared in the descending thin limb (DTL) on F16 and in the MCD on F18. After birth, NKCC2-positive TALs disappeared gradually from the tip of the renal papilla, becoming completely undetectable in the inner medulla on P21. TonEBP shifted from the cytoplasm to the nucleus in both vascular endothelial cells and MCD cells on P1, and its abundance increased gradually afterward. Immunoreactivity for AR and UT-A in the renal medulla increased markedly after birth. Treatment of neonatal animals with furosemide dramatically reduced expression of TonEBP, AR, and UT-A1. Furosemide also prevented the disappearance of NKCC2-expressing TALs in the papilla. The sequential expression of NKCC2, TonEBP, and its targets AR and UT-A and the reduced expression TonEBP and its targets in response to furosemide treatment support the hypothesis that local hypertonicity produced by the activity of NKCC2 activates TonEBP during development.

    Sequential expression of NKCC2, TonEBP, aldose reductase, and urea transporter-A in developing mouse kidney. Publishing Authors By Initials

    hw leeHW Lee,wy kimWY Kim,hk songHK Song,cw yangCW Yang,kh hanKH Han,hm kwonHM Kwon,j kimJ Kim,

    For similar water research abstracts see: water research

    PUBMED ID PMID:

    MEDLINE DATE:

    Sequential expression of NKCC2, TonEBP, aldose reductase, and urea transporter-A in developing mouse kidney. Journal Published:

    PUBLICATION TYPE: Research Support, Non-U.S. Gov

    Journal: American journal of physiology. Renal physiology

    VOLUME: 292

    Page Numbers: F269-77

    Journal Abbreviation: Am. J. Physiol. Renal Physiol.

    ISSN: 0363-6127

    DAY: 22

    MONTH: 08

    YEAR: 2006

    Sequential expression of NKCC2, TonEBP, aldose reductase, and urea transporter-A in developing mouse kidney. Information

    Number of References:

    LANGUAGE: eng

    NlmUniqueID: 100901990

    Sequential expression of NKCC2, TonEBP, aldose reductase, and urea transporter-A in developing mouse kidney. Keywords Mesh Terms:

    KEYWORDS: Water

    MESH TERMS: metabolism

    Chemical & Substance for Abstract: Sequential expression of NKCC2, TonEBP, aldose reductase, and urea transporter-A in developing mouse kidney. Information

    Substance Name: Aldehyde Reductase

    Registry Number: EC 1.1.1.21

    Grant and Affiliation Information for Sequential expression of NKCC2, TonEBP, aldose reductase, and urea transporter-A in developing mouse kidney.

    AFFILIATION: Department of Anatomy, College of Medicine, The Catholic University of Korea, Seoul.

    Country: United States

    United States Research PublicationUnited States Research Publication

    AGENCY: United States NIDDK

    GRANT: DK-42479

    ACRONYM: DK

    MEDLINETA: Am J Physiol Renal Physiol

    REFSOURCE:

    DATABASENAME:

    ACCESSION NUMBER:

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