title: 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(3)(-) 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(3)(-) (but not Cl(-)/OH(-)) exchange activity that was inhibited by DIDS but not by dibenzamidostilbene disulfonic acid (DBDS). AT-1 cell Cl(-)/HCO(3)(-) 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(3)(-) exchange activity in an atrial cell type.
authors.affiliation: Harvard-Thorndike Institute of Electrophysiology, Cardiovascular Division, Molecular Medicine and Renal Units, Beth Israel Deaconess Medical Center, Boston, MA 02215, USA.
authors.forename: P
authors.initials: P
authors.lastname: Papageorgiou
authors.forename: B E
authors.initials: BE
authors.lastname: Shmukler
authors.forename: A K
authors.initials: AK
authors.lastname: Stuart-Tilley
authors.forename: L
authors.initials: L
authors.lastname: Jiang
authors.forename: S L
authors.initials: SL
authors.lastname: Alper
mesh_terms: D017878:4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid / Q000494:pharmacology; D012856:4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfonic Acid / Q000031:analogs & derivatives* / Q000494:pharmacology; D000136:Acid-Base Equilibrium / Q000187:drug effects / Q000502:physiology; D000255:Adenosine Triphosphate / Q000494:pharmacology; D000804:Angiotensin II / Q000494:pharmacology; D000818:Animals; D027321:Anion Transport Proteins; D000838:Anions / Q000378:metabolism; D017920:Antiporters / Q000032:analysis / Q000235:genetics* / Q000378:metabolism*; D001692:Biological Transport / Q000187:drug effects / Q000502:physiology; D027963:Chloride-Bicarbonate Antiporters; D005110:Extracellular Space / Q000378:metabolism; D005260:Female; D015870:Gene Expression / Q000502:physiology; D006325:Heart Atria / Q000166:cytology; D006706:Homeostasis / Q000187:drug effects / Q000502:physiology; D007150:Immunohistochemistry; D008565:Membrane Proteins / Q000032:analysis / Q000235:genetics / Q000378:metabolism; D051379:Mice; D008815:Mice, Inbred Strains; D009206:Myocardium / Q000737:chemistry / Q000166:cytology* / Q000378:metabolism*; D019899:Paracrine Communication / Q000187:drug effects / Q000502:physiology; D012333:RNA, Messenger / Q000032:analysis; D064606:SLC4A Proteins; D012964:Sodium / Q000494:pharmacology; D014158:Transcription, Genetic / Q000502:physiology; D014407:Tumor Cells, Cultured; D014662:Vasoconstrictor Agents / Q000494:pharmacology
chemical_list: D027321:Anion Transport Proteins; D000838:Anions; D017920:Antiporters; D027963:Chloride-Bicarbonate Antiporters; D008565:Membrane Proteins; D012333:RNA, Messenger; D064606:SLC4A Proteins; C062002:Slc4a3 protein, mouse; D014662:Vasoconstrictor Agents; D000804:Angiotensin II; D012856:4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfonic Acid; C036010:4,4'-dibenzamido-2,2'-stilbenedisulfonic acid; D000255:Adenosine Triphosphate; D012964:Sodium; D017878:4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid