Skip Navigation



NDT Advance Access published online on May 21, 2008

Nephrology Dialysis Transplantation, doi:10.1093/ndt/gfn291
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow All Versions of this Article:
23/11/3397    most recent
gfn291v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Lu, P.
Right arrow Articles by Hoenderop, J. G.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Lu, P.
Right arrow Articles by Hoenderop, J. G.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© The Author [2008]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org



The β-glucuronidase klotho exclusively activates the epithelial Ca2+ channels TRPV5 and TRPV6

Peng Lu, Sandor Boros, Qing Chang, René J. Bindels and Joost G. Hoenderop

Department of Physiology, Nijmegen Centre for Molecular Life Sciences, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands

Correspondence and offprint requests to: Joost G. Hoenderop, 286 Physiology, PO Box 9101, 6500 HB Nijmegen, The Netherlands. Tel: +31-24-3610580; Fax: +31-24-3616413; E-mail: j.hoenderop{at}ncmls.ru.nl



  Abstract

Background. Active Ca2+ reabsorption in the kidney is facilitated by the epithelial transient receptor potential vanilloid Ca2+ channel subtype 5 (TRPV5). The complex-glycosylated TRPV5 is expressed at the apical membrane of the renal distal convoluted tubule (DCT) cells where the pro-urine hormone klotho can stimulate its activity by N-oligosaccharide hydrolysis. This study investigates whether klotho and its closely related analogue, β-glucuronidase, can activate other renal ion channels than TRPV5 expressed by DCT cells.

Methods. To determine the specificity of this stimulatory effect of klotho and β-glucuronidase, a selection of ion channels and transporters expressed in the kidney (TRPV4, TRPV5, TRPV6 and TRPM6) was screened in transfected HEK293 cells by using Ca2+-influx measurements.

Results. Klotho and β-glucuronidase have been found to significantly increase the activity of TRPV5 and TRPV6, but had no effect on TRPV4 and TRPM6. Furthermore, deglycosylation by endoglycosidase-F also stimulated the activity of TRPV4, TRPV5 and TRPV6, but not of TRPM6.

Conclusions. These results suggest a modulating effect for klotho primarily restricted to the epithelial Ca2+ channels TRPV5 and TRPV6.

Keywords: endoF; epithelial calcium channel; β-glucuronidase; klotho; N-glycosylation

Received for publication: 1.10.07
Accepted in revised form: 24. 4.08


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
Mol. Pharmacol.Home page
S.-K. Cha, M.-C. Hu, H. Kurosu, M. Kuro-o, O. Moe, and C.-L. Huang
Regulation of Renal Outer Medullary Potassium Channel and Renal K+ Excretion by Klotho
Mol. Pharmacol., July 1, 2009; 76(1): 38 - 46.
[Abstract] [Full Text] [PDF]


Home page
Mol. Pharmacol.Home page
J. Vriens, G. Appendino, and B. Nilius
Pharmacology of Vanilloid Transient Receptor Potential Cation Channels
Mol. Pharmacol., June 1, 2009; 75(6): 1262 - 1279.
[Abstract] [Full Text] [PDF]



Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.