title: The involvement of ZnT-1, a new modulator of cardiac L-type calcium channels, in [corrected] atrial tachycardia remodeling. [corrected].
abstract: Atrial fibrillation (AF), the highest occurring cardiac arrhythmia in the Western world, is associated with substantial morbidity and increased mortality. In spite of extensive research, the cause of atrial electrical remodeling, a major factor in the self-perpetuating nature of AF, is still unknown. Downregulation of L-type Ca2+ channel (LTCC) activity is the hallmark of atrial electrical remodeling. ZnT-1 is a ubiquitous membrane protein that was recently suggested to inhibit the LTCC. We have studied and shown that ZnT-1 expression inhibits LTCC function in an oocyte expression system as well as in isolated cardiomyocytes. Our data also show that rapid electrical pacing can augment ZnT-1 expression in culture as well as in the atria of rats in vivo. Finally, in a pilot study, ZnT-1 expression was found to be augmented in the atria of AF patients. These findings position ZnT-1 as a probable missing link in the mechanism underlying atrial tachycardia remodeling.
authors.affiliation: Department of Physiology, Faculty of Health Sciences, Ben-Gurion University of the Negev, Beer-Sheva, Israel.
authors.forename: Ofer
authors.initials: O
authors.lastname: Beharier
authors.forename: Yoram
authors.initials: Y
authors.lastname: Etzion
authors.forename: Shiri
authors.initials: S
authors.lastname: Levi
authors.forename: Merav
authors.initials: M
authors.lastname: Mor
authors.forename: Michal
authors.initials: M
authors.lastname: Mor
authors.forename: Shani
authors.initials: S
authors.lastname: Dror
authors.forename: Joy
authors.initials: J
authors.lastname: Kahn
authors.forename: Amos
authors.initials: A
authors.lastname: Katz
authors.forename: Arie
authors.initials: A
authors.lastname: Moran
mesh_terms: D000818:Animals; D020746:Calcium Channels, L-Type / Q000235:genetics / Q000378:metabolism*; D027682:Cation Transport Proteins / Q000378:metabolism*; D002478:Cells, Cultured; D003324:Coronary Artery Disease / Q000235:genetics / Q000378:metabolism* / Q000503:physiopathology; D004562:Electrocardiography; D005786:Gene Expression Regulation; D006339:Heart Rate; D006801:Humans; D008297:Male; D008565:Membrane Proteins / Q000235:genetics / Q000378:metabolism*; D009865:Oocytes / Q000378:metabolism; D010865:Pilot Projects; D051381:Rats; D017207:Rats, Sprague-Dawley; D013610:Tachycardia / Q000235:genetics / Q000378:metabolism* / Q000503:physiopathology; D029867:Xenopus Proteins / Q000378:metabolism*; D014982:Xenopus laevis
chemical_list: D020746:Calcium Channels, L-Type; D027682:Cation Transport Proteins; D008565:Membrane Proteins; C548550:SLC30A1 protein, Xenopus; C498299:SLC30A1 protein, human; D029867:Xenopus Proteins; C092392:Slc30a1 protein, rat