In vivo role of CLC chloride channels in the kidney

被引:57
作者
Uchida, S [1 ]
机构
[1] Tokyo Med & Dent Univ, Dept Internal Med 2, Sch Med, Tokyo 1138519, Japan
关键词
knockout mice; immunohistochemistry; nephrogenic diabetes insipidus; Bartter's syndrome; Dent's disease;
D O I
10.1152/ajprenal.2000.279.5.F802
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
Chloride channels in the kidney are involved in important physiological functions such as cell volume regulation, acidification of intracellular vesicles, and transepithelial chloride transport. Among eight mammalian CLC chloride channels expressed in the kidney, three (CLC-K1, CLC-K2, and CLC-5) were identified to be related to kidney diseases in humans or mice. CLC-K1 mediates a transepithelial chloride transport in the thin ascending limb of Henle's loop and is essential for urinary concentrating mechanisms. CLC-K2 is a basolateral chloride channel in distal nephron segments and is necessary for chloride reabsorption. CLC-5 is a chloride channel in intracellular vesicles of proximal tubules and is involved in endocytosis. This review will cover the recent advances in research on the CLC chloride channels of the kidney with a special focus on the issues most necessary to understand their physiological roles in vivo, i. e., their intrarenal and cellular localization and their phenotypes of humans and mice that have their loss-of-function mutations.
引用
收藏
页码:F802 / F808
页数:7
相关论文
共 52 条
[1]  
ADACHI S, 1994, J BIOL CHEM, V269, P17677
[2]   Mutations of CLCN5 in Japanese children with idiopathic low molecular weight proteinuria, hypercalciuria and nephrocalcinosis [J].
Akuta, N ;
Lloyd, SE ;
Igarashi, T ;
Shiraga, H ;
Matsuyama, T ;
Yokoro, S ;
Cox, JPD ;
Thakker, RV .
KIDNEY INTERNATIONAL, 1997, 52 (04) :911-916
[3]   ClC-6 and ClC-7 are two novel broadly expressed members of the CLC chloride channel family [J].
Brandt, S ;
Jentsch, TJ .
FEBS LETTERS, 1995, 377 (01) :15-20
[4]   Evidence for the intracellular location of chloride channel (CIC)-type proteins:: co-localization of CIC-6a and CIC-6c with the sarco/endoplasmic-reticulum Ca2+ pump SERCA2b [J].
Buyse, G ;
Trouet, D ;
Voets, T ;
Missiaen, L ;
Droogmans, G ;
Nilius, B ;
Eggermont, J .
BIOCHEMICAL JOURNAL, 1998, 330 :1015-1021
[5]   Intra-renal and subcellular distribution of the human chloride channel, CLC-5, reveals a pathophysiological basis for Dent's disease [J].
Devuyst, O ;
Christie, PT ;
Courtoy, PJ ;
Beauwens, R ;
Thakker, RV .
HUMAN MOLECULAR GENETICS, 1999, 8 (02) :247-257
[6]   Molecular identification of a volume-regulated chloride channel [J].
Duan, D ;
Winter, C ;
Cowley, S ;
Hume, JR ;
Horowitz, B .
NATURE, 1997, 390 (6658) :417-421
[7]   Mutational analysis demonstrates that ClC-4 and ClC-5 directly mediate plasma membrane currents [J].
Friedrich, T ;
Breiderhoff, T ;
Jentsch, TJ .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1999, 274 (02) :896-902
[8]   The yeast CLC chloride channel functions in cation homeostasis [J].
Gaxiola, RA ;
Yuan, DS ;
Klausner, RD ;
Fink, GR .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1998, 95 (07) :4046-4050
[9]   THE GEF1 GENE OF SACCHAROMYCES-CEREVISIAE ENCODES AN INTEGRAL MEMBRANE-PROTEIN - MUTATIONS IN WHICH HAVE EFFECTS ON RESPIRATION AND IRON-LIMITED GROWTH [J].
GREENE, JR ;
BROWN, NH ;
DIDOMENICO, BJ ;
KAPLAN, J ;
EIDE, DJ .
MOLECULAR AND GENERAL GENETICS, 1993, 241 (5-6) :542-553
[10]   ClC-5, the chloride channel mutated in Dent's disease, colocalizes with the proton pump in endocytotically active kidney cells [J].
Günther, W ;
Lüchow, A ;
Cluzeaud, F ;
Vandewalle, A ;
Jentsch, TJ .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1998, 95 (14) :8075-8080