MicroRNA-1、29a、133a In Persistent Atrial Fibrillation Dog Model Of The Expressions Of Atrial Muscle Changes

Object: To investigate the MicroRNA-1、29a、133a gene expression in atrial and toevaluate the influence of MicroRNA-1、29a、133a expression on AF and fibrosis. Methods:The chronic rapid atrial pacing was used to establish the persistent AF dog model and thesham-operated group was seted. Application of cardiac ultrasound measurement of thecardiac structure size, masson three color staining was used to determine the stage offibrosis, the expression the left atrial(LA) MicroRNA-1、29a、133a mRNA level wasdetected through reverse transcriptase polymerase chain reaction. Results: Persistent atrialfibrillation model in dogs after modeling and model compared to the former, atrialdilatation, decreased ejection fraction, but the difference was not statistically significant (P＞0.05), compared with sham-operated group, the degree of fibrosis and collagen volumefraction (CVF) in persistent AF model group was increased obviously (P＜0.05), and theexpression microRNA-1mRNA was increased obviously (P＜0.05). The level ofmicroRNA-29a、-133a mRNA expression was decreased obviously (P＜0.01，P＜0.05).Conclusion: Atrial structural remodeling and atrial fibrosis is atrial fibrillation andmaintain the essential matrix, in the persistent atrial fibrillation (af) model of dog atrialorganization, and heighten of microRNA-1activity and microRNA-29a、-133a reduce ofactivity may influence collagen metabolism, promoting or inhibiting the myocardialfibrosis, it is one of the molecular mechanism that cause the reconstruction of atrialstructure in atrial fibrillation.