Connexin 43 participates in atrial electrical remodelling through colocalization with calcium channels in atrial myocytes.
De-Wei PengYing-Yu LaiXue-Shan LuoXin LiChun-Yu DengHui-Ming GuoJun-Fei ZhaoHui YangYang LiuZhao-Yu WangYu-Wen XuSu-Juan KuangShu-Lin WuYu-Mei XueFang RaoPublished in: Clinical and experimental pharmacology & physiology (2021)
Atrial fibrillation (AF) is associated with atrial conduction disturbances caused by electrical and/or structural remodelling. In the present study, we hypothesized that connexin might interact with the calcium channel through forming a protein complex and, then, participates in the pathogenesis of AF. Western blot and whole-cell patch clamp showed that protein levels of Cav1.2 and connexin 43 (Cx43) and basal ICa , L were decreased in AF subjects compared to sinus rhythm (SR) controls. In cultured atrium-derived myocytes (HL-1 cells), knocking-down of Cx43 or incubation with 30 mmol/L glycyrrhetinic acid significantly inhibited protein levels of Cav1.2 and Cav3.1 and the current density of ICa , L and ICa , T . Incubation with nifedipine or mibefradil decreased the protein level of Cx43 in HL-1 cells. Moreover, Cx43 was colocalized with Cav1.2 and Cav3.1 in atrial myocytes. Therefore, Cx43 might regulate the ICa , L and ICa , T through colocalization with calcium channel subunits in atrial myocytes, representing a potential pathogenic mechanism in AF.
Keyphrases
- atrial fibrillation
- catheter ablation
- left atrial
- left atrial appendage
- oral anticoagulants
- direct oral anticoagulants
- induced apoptosis
- heart failure
- protein protein
- percutaneous coronary intervention
- amino acid
- binding protein
- stem cells
- cell cycle arrest
- coronary artery disease
- single cell
- south africa
- endothelial cells
- cell death
- oxidative stress
- coronary artery
- climate change
- inferior vena cava
- pi k akt