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CLOPRESS

Renal Chloride Chanels and Blood Pressure Regulation

Total Cost €

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EC-Contrib. €

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Partnership

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Project "CLOPRESS" data sheet

The following table provides information about the project.

Coordinator
INSTITUT NATIONAL DE LA SANTE ET DE LA RECHERCHE MEDICALE 

Organization address
address: RUE DE TOLBIAC 101
city: PARIS
postcode: 75654
website: www.inserm.fr

contact info
title: n.a.
name: n.a.
surname: n.a.
function: n.a.
email: n.a.
telephone: n.a.
fax: n.a.

 Coordinator Country France [FR]
 Project website http://parcc.inserm.fr/spip.php
 Total cost 173˙076 €
 EC max contribution 173˙076 € (100%)
 Programme 1. H2020-EU.1.3.2. (Nurturing excellence by means of cross-border and cross-sector mobility)
 Code Call H2020-MSCA-IF-2014
 Funding Scheme MSCA-IF-EF-ST
 Starting year 2015
 Duration (year-month-day) from 2015-05-01   to  2017-04-30

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    INSTITUT NATIONAL DE LA SANTE ET DE LA RECHERCHE MEDICALE FR (PARIS) coordinator 173˙076.00

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 Project objective

Hypertension, or elevated arterial blood pressure, is a significant global health concern. A major cause of hypertension is the abnormality in salt (NaCl) handling in distal nephron segments within kidney. Although there has been long a debate with regard to the relative importance of Na vs. Cl- in inducing salt-sensitive hypertension, previous research demonstrated that excess intake of Cl- could lead to severe salt-sensitive hypertension. Thus, better understanding on molecular mechanisms of renal Cl- handling would provide useful insights in treatment of hypertension. Previous studies largely focused on the identification and regulation of apically expressed Cl- transporters, including Na-Cl- cotransporter, Na-K-2Cl- cotransporter (NKCC1/NKCC2) and pendrin, but mechanisms and regulation of Cl- transporters on basolateral membranes (i.e. an exit of Cl- into the interstitial space) remains poorly described. Thus, the current proposal will investigate the physiological role of basolateral Cl- channel distributed in distal nephron, specifically ClC-kb. Using a transgenic ClC-kb knockout line of mice, I propose to investigate the physiological role of this channel within isolated tubule and at the whole animal level. In addition, ClC-kb channel is known to interact with a functional β-subunit, barttin, and this interaction could affect Cl- conductance. I propose to investigate the molecular mechanisms by which barttin can affect ClC-kb-mediated chloride transport. The proposed studies will shed new insights into the molecular mechanisms of Cl- reabsorption in distal nephron, and could provide a basis for novel approach in treatment of hypertension.

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