ISSN 2149-2263 | E-ISSN 2149-2271
The Anatolian Journal of Cardiology
Desmosomal Junctions and Connexin-43 Remodeling in High-Pacing-Induced Heart Failure Dogs [Anatol J Cardiol]
Anatol J Cardiol. 2023; 27(8): 462-471 | DOI: 10.14744/AnatolJCardiol.2023.2823

Desmosomal Junctions and Connexin-43 Remodeling in High-Pacing-Induced Heart Failure Dogs

Qing Wang, Liang Xiaoyan, Shuai Shang, Yongqiang Fan, Huasheng Lv, Baopeng Tang, Yanmei Lu
Department of Pacing and Electrophysiology, The First Affiliated Hospital of Xinjiang Medical University, Xinjiang, China; Xinjiang Key Laboratory of Cardiac Electrophysiology and Cardiac Remodeling, The First Affiliated Hospital of Xinjiang Medical University, Xinjiang, China

Background: While desmosomal junctions and gap junction remodeling are among the arrhythmogenic substrates, the fate of desmosomal and gap junctions in high-pacing-induced heart failure remains unclear. This aim of this study was to determine the fate of desmosomal junctions in high-pacing-induced heart failure.

Methods: Dogs were randomly divided into 2 equal groups, a high-pacing-induced heart failure model group (heart failure group, n = 6) and a sham operation group (control group, n = 6). Echocardiography and cardiac electrophysiological examination were performed. Cardiac tissue was analyzed by immunofluorescence and transmission electron microscopy. The expression of desmoplakin and desmoglein-2 proteins was detected by western blot.

Results: A significant decrease in ejection fraction, significant cardiac dilatation, diastolic and systolic dysfunction, and ventricular thinning occurred after 4 weeks in high-pacing-induced dog model of heart failure. Effective refractory period action potential duration at 90% repolarization was prolonged in the heart failure group. Immunofluorescence analysis and transmission electron microscopy demonstrated connexin-43 lateralization accompanies desmoglein-2 and desmoplakin remodeling in the heart failure group. Western blotting showed that the expression of desmoplakin and desmoglein-2 proteins was higher in heart failure than in normal tissue.

Conclusion: Desmosome (desmoglein-2 and desmoplakin) redistribution and desmosome (desmoglein-2) overexpression accompanying connexin-43 lateralization were parts of a complex remodeling in high–pacing-induced heart failure.

Keywords: Connexin-43, desmosomes, gap junction, heart failure

Qing Wang, Liang Xiaoyan, Shuai Shang, Yongqiang Fan, Huasheng Lv, Baopeng Tang, Yanmei Lu. Desmosomal Junctions and Connexin-43 Remodeling in High-Pacing-Induced Heart Failure Dogs. Anatol J Cardiol. 2023; 27(8): 462-471

Corresponding Author: Yanmei Lu
Manuscript Language: English


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