AE anion exchangers in atrial tumor cells

Abstract

Intracellular pH homeostasis and intracellular Cl−concentration in cardiac myocytes are regulated by anion exchange mechanisms. In physiological extracellular Cl−concentrations, Cl−/HCO[Formula: see text] exchange promotes intracellular acidification and Cl−loading sensitive to inhibition by stilbene disulfonates. We investigated the expression of AE anion exchangers in the AT-1 mouse atrial tumor cell line. Cultured AT-1 cells exhibited a substantial basal Na+-independent Cl−/HCO[Formula: see text] (but not Cl−/OH−) exchange activity that was inhibited by DIDS but not by dibenzamidostilbene disulfonic acid (DBDS). AT-1 cell Cl−/HCO[Formula: see text] activity was stimulated two- to threefold by extracellular ATP and ANG II. AE mRNAs detected by RT-PCR in AT-1 cells included brain AE3 (bAE3), cardiac AE3 (cAE3), AE2a, AE2b, AE2c1, AE2c2, and erythroid AE1 (eAE1), but not kidney AE1 (kAE1). Cultured AT-1 cells expressed AE2, cAE3, and bAE3 polypeptides, which were detected by immunoblot and immunocytochemistry. An AE1-like epitope was detected by immunocytochemistry but not by immunoblot. Both bAE3 and cAE3 were present in intact AT-1 tumors. Cultured AT-1 cells provide a useful system for the study of mediators and regulators of Cl−/HCO[Formula: see text] exchange activity in an atrial cell type.