Open AccessAnti-Ro52 antibody acts on the S5-pore linker of hERG to chronically reduce channel expression
Author(s) -
John A. Szendrey,
Shawn M. Lamothe,
S Vanner,
Jun Guo,
Tonghua Yang,
Wentao Li,
Jordan H. Davis,
M. G. Joneja,
Adrián Baranchuk,
Shetuan Zhang
Publication year - 2018
Publication title -
cardiovascular research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.774
H-Index - 219
eISSN - 1755-3245
pISSN - 0008-6363
DOI - 10.1093/cvr/cvy310
Subject(s) - herg , potassium channel , pharmacology , hek 293 cells , autoantibody , patch clamp , antibody , chemistry , microbiology and biotechnology , medicine , biology , electrophysiology , immunology , receptor
The human ether-a-go-go-related gene (hERG) encodes the rapidly activating delayed rectifier potassium channel (IKr). Malfunction of hERG/IKr is the primary cause of acquired long QT syndrome (LQTS), an electrical disorder of the heart that can cause arrhythmias and sudden death. Patients with autoimmune diseases display a high incidence of LQTS. While dysfunction of hERG channels induced by autoantibodies such as anti-Ro52 may play a role in this pathology, the underlying mechanisms are not well understood. Here, we investigated the acute and chronic effects of anti-Ro52 antibody on hERG channels stably expressed in human embryonic kidney (hERG-HEK) 293 cells as well as IKr in neonatal rat ventricular myocytes.