Down-regulation of the Human Ether-a-go-go-Related Gene in Rat Cardiac Hypertrophy

Transmural dispersion of repolarization and cardiac remodeling in ventricles of rabbit with right ventricular hypertrophy

“…The hERG mRNA expression was higher in the endocardium of both left and right ventricles of rabbits with RVH than those of SHAM rabbits. These results yield both agree and disagree with previous studies (Han, Chartier, Li, & Nattel, 2001;Hu, Yan, Lin, Liu, & Li, 2011;Li, Lau, Ducharme, Tardif, & Nattel, 2002;Tsuji et al, 2000). The findings of I Kr in disease heart are variable which could be due to the difference in species, the different zones of the heart (i.e., apex vs base, epicardium vs midmyocardium vs endocardium), and types of heart disease (Li et al, 2002;Panyasing et al, 2010;Tsuji, Zicha, Qi, Kodama, & Nattel, 2006;Volders et al, 1999).…”

“…Other studies demonstrated that I Kr was not changed in canine heart failure (Han et al, 2001;Li et al, 2002). In rats with left ventricular hypertrophy, the down-regulation of hERG mRNA expression was reported (Hu et al, 2011). Previous study has compared the expression of hERG and KvLQT1 (an I Ks channel encoded by KCNQ1 gene) mRNA expression between tachypaced rabbits and bradypaced rabbits and found that hERG mRNA was downregulated only in bradypaced rabbits whereas KvLQT1 mRNA was downregulated in both groups (Tsuji et al, 2006).…”

hERG K+Channels: Structure, Function, and Clinical Significance

“…This does not, however, preclude the possibility that there are changes in the level of hERG protein or Kv11.1 current density. In a rat model of cardiac hypertrophy, which is a precursor to heart failure, it has been reported that KCNH2 mRNA and protein levels are decreased (277). This is not necessarily incompatible with the data from McDonald et al showing that chronic (24 h) neurohormonal stimulation of myocytes leads to increased hERG protein synthesis, as in heart failure chronic stimulation usually leads to downregulation of signaling pathways (348).…”

Stimulation of HERG Channel Activity by β-catenin

“…As a matter of fact, cardiac hypertrophy is paralleled by enhanced ß-catenin abundance and activity. However, HERG channels have been described to be downregulated in cardiac hypertrophy [30], [41], an effect mediated by mechanisms other than ß-catenin, such as activation of AT 1 receptors with subsequent activation of protein kinase C linked to the PKC pathway in ventricular myocytes [42].…”