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 Scijournal_title
Life sciencesauthors
Simão S,Gomes P,Pinho MJ,Soares-da-Silva Pdoi
10.1016/j.lfs.2013.07.026subject
Has Abstractpub_date
2013-10-06 00:00:00pages
435-40issue
12-14eissn
0024-3205issn
1879-0631pii
S0024-3205(13)00441-4journal_volume
93pub_type
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