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Harvard-Thorndike Institute of Electrophysiology, Cardiovascular Division, Molecular Medicine and Renal Units, Beth Israel Deaconess Medical Center, Boston; and Departments of Medicine and Cell Biology, Harvard Medical School, Boston, Massachusetts 02215
Intracellular pH
homeostasis and intracellular Cl
concentration in cardiac
myocytes are regulated by anion exchange mechanisms. In physiological
extracellular Cl
concentrations,
Cl
/HCO
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
(but not
Cl
/OH
) exchange activity that was inhibited
by DIDS but not by dibenzamidostilbene disulfonic acid (DBDS). AT-1
cell Cl
/HCO
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
exchange activity in an atrial
cell type.
AT-1; band 3; AE1; AE3; chloride-bicarbonate exchange; atrium; heart
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