Modulative effects of lncRNA TCONS_00202959 on autonomic neural function and myocardial functions in atrial fibrillation rat model.

Abstract

Atrial fibrillation (AF) is a typical cardiac arrhythmia. The autonomic nervous system can modulate the myocardial system with complicated mechanisms. Long non-coding RNA (lncRNA) is involved in myocardial diseases, and lncRNA TCONS_00202959 is down-regulated in AF. However, the detailed effects of AF on automatic functions or cardiomyocytes are not well known yet. Sprague-Dawley (SD) rats were randomly divided into control group, AF group (which was prepared by injecting the acetylcholine-CaCl2 solution) and treatment group (receiving lentiviral transfection of lncRNA TCONS_00202959 on AF rats). Real Time-quantitative PCR (RT-PCR) was used to measure the expression of lncRNA TCONS_00202959. Atrial effective refractory period (AERP) and AF induction rate were measured, along with heart rate variability (HRV) analysis to reveal autonomic nervous function. The expression of tyrosine hydroxylase (TH) and choline acetyltransferase (CHAT) was analyzed in atrial tissues. The expression of lncRNA TCONS_00202959 was decreased in the AF group compared to the control group (p < 0.05), which also had shortened AERP and elevated AF induction rate. The analysis of the autonomic nervous function revealed lower standard deviation of NN intervals (SDNN), SDNN of atrial (SDANN), root mean square of successive differences (RMSSD) and SDNN intervals in all 5-min segments (SDNNindx), plus elevated power ratio of low frequency (LF)/high frequency (HF). TH expression was increased whilst CHAT expression was decreased (p < 0.05). The treatment group showed enhanced expression of lncRNA TCONS_00202959, elongated AERP plus decreased AF induction rate. The treatment rats also had higher SDNN, SDANN, RMSSD and SDNNindx, lower LF/HF ratio, decreased TH expression and increased CHAT expression (p < 0.05 compared to the AF group). AF rats had decreased expression of lncRNA TCONS_00202959, which can help to prevent AF pathogenesis by suppressing cardiac autonomic nervous function.