Identification of SLC26A transporters involved in the Cl⁻/HCO₃⁻ exchange in proximal tubular cells from WKY and SHR.

Abstract:

AIMS:slc26a proteins are responsible for a large number of functions either in normal physiology or in human disease. We have previously reported that proximal tubular epithelial (PTE) cells immortalized from spontaneously hypertensive rats (SHRs) were endowed with increased Cl(-)/HCO3(-) exchanger activity and slc26a6 protein expression compared with PTE cells immortalized from normotensive Wistar Kyoto (WKY) rats. The aim of the present study was to identify slc26a members responsible for the Cl(-)/HCO3(-) exchange in WKY and SHR PTE cells. MAIN METHODS:Cl(-)/HCO3(-) exchanger activity was assessed as the initial rate of pHi recovery after removal of HCO3(-) or after removal of Cl(-). The presence of slc26a genes was evaluated by means of reverse transcriptase-PCR (RT-PCR) in WKY and SHR PTE cell lines and in the kidney of WKY and SHR. Transcript abundance was measured by quantitative real-time polymerase chain reaction (PCR). KEY FINDINGS:We detected slc26a4, slc26a6, slc26a7 and slc26a9 transcripts in the rat kidney of WKY and SHR. In WKY and SHR PTE cell lines we detected slc26a4, slc26a6 and slc26a9 transcripts, which were, respectively, 12-, 4- and 15-fold upregulated in SHR cells. Gene silencing with small interfering RNAs (siRNAs) targeting slc26a4, slc26a6 and slc26a9 reduced Cl(-)/HCO3(-) exchanger activity in both cell lines. SIGNIFICANCE:These results indicate that Cl(-)/HCO3(-) exchanger activity is mediated by, at least in part, slc26a4, slc26a6 and slc26a9 in cultured WKY and SHR cells. The overexpression of these slc26a members in SHR cells may correspond to an adaptive process to cope with the sustained increase in proximal tubular sodium reabsorption.

journal_name

Life Sci

journal_title

Life sciences

authors

Simão S,Gomes P,Pinho MJ,Soares-da-Silva P

doi

10.1016/j.lfs.2013.07.026

subject

Has Abstract

pub_date

2013-10-06 00:00:00

pages

435-40

issue

12-14

eissn

0024-3205

issn

1879-0631

pii

S0024-3205(13)00441-4

journal_volume

93

pub_type

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