Document Detail


Hypertonicity increases CLC-5 expression in mouse medullary thick ascending limb cells.
MedLine Citation:
PMID:  15161605     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Genetic studies indicated that mutations of the chloride channel CLC-5 in the kidney are responsible for a group of clinical disorders, collectively called Dent's disease. In the kidney, CLC-5 was found to be expressed in the proximal tubule, medullary thick ascending limb (mTAL) of loop of Henle, and intercalated cells of the collecting tubule. In proximal tubular cells, CLC-5 was found to play an important role in receptor-mediated endocytosis. However, the functional roles of CLC-5 in mTAL and collecting tubules remain unclear. Because mTAL is normally exposed to a hypertonic environment, we aimed to examine the effect of hypertonicity on CLC-5 expression in this nephron segment. Our studies revealed that exposure to hypertonicity (up to 550 mosM) increased CLC-5 mRNA and protein levels in a murine mTAL cell line (MTAL) but not in an opossum kidney (OK) proximal tubular cell line. A similar effect was also found in mouse kidneys, where CLC-5 expression was enhanced in renal medulla, but not cortex, after 48 h of water deprivation. We also tested the effect of hypertonicity on endocytotic activity and found that exposure to hypertonicity caused a significant decrease in cellular uptake of FITC-labeled albumin in OK but not in MTAL cells. Our results suggest that CLC-5 expression is upregulated by hypertonicity in mTAL cells but not in proximal tubular cells. We speculate that the increased CLC-5 levels in mTAL may serve to maintain the endocytotic activity in a hypertonic environment.
Authors:
Phuong-Chi Pham; Olivier Devuyst; Phuong-Thu Pham; Naoko Matsumoto; Remi N G Shih; Oak D Jo; Norimoto Yanagawa; Adam M Sun
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.     Date:  2004-05-25
Journal Detail:
Title:  American journal of physiology. Renal physiology     Volume:  287     ISSN:  1931-857X     ISO Abbreviation:  Am. J. Physiol. Renal Physiol.     Publication Date:  2004 Oct 
Date Detail:
Created Date:  2004-09-03     Completed Date:  2004-10-25     Revised Date:  2011-04-28    
Medline Journal Info:
Nlm Unique ID:  100901990     Medline TA:  Am J Physiol Renal Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  F747-52     Citation Subset:  IM    
Affiliation:
Renal Division, Department of Medicine, Olive View-UCLA Medical Center, Sylmar, CA 91342, USA. pctp@ucla.edu
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MeSH Terms
Descriptor/Qualifier:
Animals
Cells, Cultured
Chloride Channels / genetics*,  metabolism*
Endocytosis / physiology
Gene Expression
Hypertonic Solutions / pharmacology
Kidney Tubules, Proximal / cytology
Loop of Henle / cytology,  physiology*
Male
Mice
Mice, Inbred C57BL
Opossums
RNA, Messenger / metabolism
Water Deprivation / physiology*
Grant Support
ID/Acronym/Agency:
DK-47403/DK/NIDDK NIH HHS; R01-DK-58886/DK/NIDDK NIH HHS
Chemical
Reg. No./Substance:
0/CLC-5 chloride channel; 0/Chloride Channels; 0/Hypertonic Solutions; 0/RNA, Messenger

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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