title: Increased acid load and deletion of AE1 increase Slc26a7 expression.
abstract: OBJECTIVE
  Slc26a7 is a member of a family of anion transport proteins, Solute-Linked Carrier 26 (Slc26). Slc26a7, which can mediate Cl-/HCO3- exchange, is expressed in the acid-secreting, A-intercalated cells of the kidney collecting duct. On the basolateral side of the A-intercalated cells, Slc26a7 co-localizes with the anion exchanger 1 (AE1), a Cl-/HCO3- exchanger that mediates bicarbonate reabsorption in the collecting duct.
  
  
  METHODS
  To test if Slc26a7 is involved in acid-base regulation, as its localization and function suggest, we examined the effect of acid loading and deletion of AE1 on Slc26a7 expression with quantitative real-time RT-PCR and Western blotting.
  
  
  RESULTS
  Four days of acid loading increased Slc26a7 mRNA expression in the kidney inner medulla by 57% (n = 6 acid loaded vs. n = 6 control rats; p < 0.001), whereas mRNA expression in the outer medulla and the cortex did not change. Western blotting analysis demonstrated increased Slc26a7 protein expression in both outer (140%) and inner medulla (50%) in acid-loaded animals (n = 3) compared to controls (n = 3; p < 0.05). The expression of Slc26a7 mRNA was increased by 66% in the kidneys of AE1 knockout mice (n = 5) compared to the wild types (n = 5, p < 0.001). The increase in Slc26a7 mRNA correlated with a twofold increase in protein expression (p < 0.05).
  
  
  CONCLUSIONS
  We suggest that the increase in Slc26a7 expression caused by acid challenge and deletion of AE1 represents an adaptive response, indicating that Slc26a7 contributes to the regulation of acid-base balance by the kidney.
authors.affiliation: Department of Medicine, University of Cincinnati, Cincinnati, Ohio 45267-0585, USA.
authors.forename: Xuming
authors.initials: X
authors.lastname: Sun
authors.forename: Snezana
authors.initials: S
authors.lastname: Petrovic
mesh_terms: D000136:Acid-Base Equilibrium; D000138:Acidosis / Q000139:chemically induced / Q000378:metabolism*; D000643:Ammonium Chloride; D000818:Animals; D001457:Anion Exchange Protein 1, Erythrocyte / Q000172:deficiency / Q000235:genetics / Q000378:metabolism*; D017920:Antiporters / Q000235:genetics / Q000378:metabolism*; D015153:Blotting, Western; D027963:Chloride-Bicarbonate Antiporters / Q000235:genetics / Q000378:metabolism*; D004195:Disease Models, Animal; D005260:Female; D007679:Kidney Medulla / Q000378:metabolism*; D051379:Mice; D018345:Mice, Knockout; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D020133:Reverse Transcriptase Polymerase Chain Reaction; D000076988:Sulfate Transporters; D015854:Up-Regulation
chemical_list: D001457:Anion Exchange Protein 1, Erythrocyte; D017920:Antiporters; D027963:Chloride-Bicarbonate Antiporters; D012333:RNA, Messenger; C486743:Slc26a7 protein, mouse; C486744:Slc26a7 protein, rat; C523515:Slc4a1 protein, mouse; D000076988:Sulfate Transporters; D000643:Ammonium Chloride