| First Author | Hong CS | Year | 2002 |
| Journal | FASEB J | Volume | 16 |
| Issue | 10 | Pages | 1310-2 |
| PubMed ID | 12154005 | Mgi Jnum | J:128770 |
| Mgi Id | MGI:3768002 | Doi | 10.1096/fj.01-0908fje |
| Citation | Hong CS, et al. (2002) Cardiac remodeling and atrial fibrillation in transgenic mice overexpressing junctin. FASEB J 16(10):1310-2 |
| abstractText | Junctin is a 26-kDa integral membrane protein, colocalized with the ryanodine receptor (RyR) and calsequestrin at the junctional sarcoplasmic reticulum (SR) membrane in cardiac and skeletal muscles. To elucidate the functional role of junctin in heart, transgenic (TG) mice overexpressing canine junctin (24-29 folds) under the control of mouse a-myosin heavy chain promoter were generated. Overexpression of the junctin in mouse heart was associated with heart enlargements, bradycardia, atrial fibrillation, and increased fibrosis. Many ultrastructural alterations were observed in TG atria. The junctional SR cisternae facing transverse-tubules contained a dense matrix of calsequestrin in TG heart. According to echocardiography, TG mice showed enlarged left ventricles, dilated right atriums, and ventricles with paradoxical septal motion and impaired left ventricular systolic function. Overexpression of junctin led to down-regulation of triadin and RyR but to up-regulation of dihydropyridine receptor. The L-type Ca2+ current density and action potential durations increased, which could be the cause for the bradycardia in TG heart. This study provides an important example of pathogenesis leading to substantial cardiac remodeling and atrial fibrillation, which was caused by overexpression of junctin in heart. |
