TY - JOUR
T1 - Correlation between atrial ZnT-1 expression and atrial fibrillation in humans
T2 - A pilot study
AU - Etzion, Yoram
AU - Ganiel, Amir
AU - Beharier, Ofer
AU - Shalev, Aryeh
AU - Novack, Victor
AU - Volvich, Liobov
AU - Abrahamov, Dan
AU - Matsa, Menachem
AU - Sahar, Gideon
AU - Moran, Arie
AU - Katz, Amos
PY - 2008/2/1
Y1 - 2008/2/1
N2 - ZnT-1 in Atrial Fibrillation. Background: Until recently, the membrane protein ZnT-1 was studied mainly in the context of zinc homeostasis. However, new findings indicate that it acts as an inhibitor of L-type calcium channels. We recently found that acute rapid pacing of the rat atria in vivo augments the expression of ZnT-1, while knockdown of ZnT-1 in culture can oppose the inhibition of L-type calcium channels following rapid pacing. This pilot study, the first to assess cardiac ZnT-1 in humans, was designed to look for possible correlation between the atrial expression of ZnT-1 and atrial fibrillation. Methods: Right atrial appendage tissue was collected from 39 patients (27 with sinus rhythm and 12 with atrial fibrillation; 6-permanent, 6- paroxysmal or persistent) undergoing open-heart surgery. The expression of ZnT-1 was analyzed by Western blot utilizing β-actin as an internal loading control and a standard rat heart sample (STD) for inter-blot comparison. Results: Overall atrial fibrillation patients (n = 12) had median ZnT-1/β-actin of 1.80 STD (inter-quartile range 1.26 to 2.85) versus 0.73 STD (0.24 to 1.64) in the sinus rhythm group (P = 0.002). No association was found between ZnT-1 level and most other clinical parameters tested. Multivariate analysis determined that atrial fibrillation and increased body mass index were the only independent variables clearly associated with higher ZnT-1 levels (Standardized coefficients Beta = 0.62, 0.31; P = 0.002, P = 0.04, respectively). Conclusions: This pilot study provides evidence for increased ZnT-1 expression in the atria of patients with atrial fibrillation.
AB - ZnT-1 in Atrial Fibrillation. Background: Until recently, the membrane protein ZnT-1 was studied mainly in the context of zinc homeostasis. However, new findings indicate that it acts as an inhibitor of L-type calcium channels. We recently found that acute rapid pacing of the rat atria in vivo augments the expression of ZnT-1, while knockdown of ZnT-1 in culture can oppose the inhibition of L-type calcium channels following rapid pacing. This pilot study, the first to assess cardiac ZnT-1 in humans, was designed to look for possible correlation between the atrial expression of ZnT-1 and atrial fibrillation. Methods: Right atrial appendage tissue was collected from 39 patients (27 with sinus rhythm and 12 with atrial fibrillation; 6-permanent, 6- paroxysmal or persistent) undergoing open-heart surgery. The expression of ZnT-1 was analyzed by Western blot utilizing β-actin as an internal loading control and a standard rat heart sample (STD) for inter-blot comparison. Results: Overall atrial fibrillation patients (n = 12) had median ZnT-1/β-actin of 1.80 STD (inter-quartile range 1.26 to 2.85) versus 0.73 STD (0.24 to 1.64) in the sinus rhythm group (P = 0.002). No association was found between ZnT-1 level and most other clinical parameters tested. Multivariate analysis determined that atrial fibrillation and increased body mass index were the only independent variables clearly associated with higher ZnT-1 levels (Standardized coefficients Beta = 0.62, 0.31; P = 0.002, P = 0.04, respectively). Conclusions: This pilot study provides evidence for increased ZnT-1 expression in the atria of patients with atrial fibrillation.
KW - Atrial fibrillation
KW - Calcium channels
KW - Cation diffusion facilitator proteins
KW - Electrical remodeling
KW - ZnT-1
UR - http://www.scopus.com/inward/record.url?scp=38949148292&partnerID=8YFLogxK
U2 - 10.1111/j.1540-8167.2007.01008.x
DO - 10.1111/j.1540-8167.2007.01008.x
M3 - Article
C2 - 17971132
AN - SCOPUS:38949148292
SN - 1045-3873
VL - 19
SP - 157
EP - 164
JO - Journal of Cardiovascular Electrophysiology
JF - Journal of Cardiovascular Electrophysiology
IS - 2
ER -