JPH2 Gene Expression In Persistent Atrial Fibrillation With Mitral Valve Disease

Objective:Atrial fibrillation and heart failure often coexist, causing substantial cardiovascular morbidity and mortality. Presently available therapeutic approaches have limited efficacy and nontrivial potential to cause adverse effects. Thus, new mechanistic knowledge is essential for therapeutic innovation. This research it to explore the JPH2 expression in persistent atrial fibrillation with mitral valve disease.Methods: This study was divided into three groups. Group A included 7 normal left atrial tissue samples that taken from the donor hearts, group B consisted of 16 patients with mitral valve disease, and group C comprised 18 patients with mitral valve disease and persistent atrial fibrillation. The left atrial tissue samples were taken from group B and C when they underwent cardiac surgery. Electron microscopy technique was used to observed ultrastructure of atrial tissue. Westernblot technique was used to test the Junctophilin-2 expression and the RT-PCR method was used to test the JP-2 gene expression.Results:The atrial myocytes from patients with AF showed remarkable changes in ultrastructure, the electron microscopy showed the obvious interstitial fibrosis. The electron microscopy also showed that the myolytic space was filled huge amounts of glycogen in almost all cells that underwent myolysis. Mitochondria increased and clustered, typical changes in size and shape of mitochondria were seen in areas depleted of sarcomeres: Many mitochondria had become elongated and were in different size. Nuclei was heterotypical and the heterochromatin was nubbly gathered throughout the nucleoplasm. Intercalated disc was asynechia and distorted seriously. Between group A and group B, there was no difference in the level of JPH2 m RNA and protein. The Westernblot results showed Junctophilin-2 versus GAPDHexpression down regulated in persistent atrial fibrillation(0.94±0.29 vs 1.53±0.61, P<0.01). However, there was no difference between atrial fibrillation patients and sinus rhythm patients(1.76±1.38 vs 1.15±0.94, P>0.05). Expression of mi RNA-24 was significantly up-regulated in patients with persistent atrial fibrillation(4.49±4.30 vs 1.72±1.08, P<0.05). There was no significant difference in mean age, gender, ejection fraction and NYHA among the two groups. But the left atrial diameter was significant larger in patients with persistent atrial fibrillation compared to those in sinus rhythm.Conclusion:Junctophilin-2 protein down-regulation may be associated with atrial fibrillation, causing left atrial remodeling and contraction dysfunction.