The Mechanism Of Endoplasmic Reticulum Stress Involved In The Occurrence Of Atrial Fibrillation

To explore the mechanism of Endoplasmic Reticulum Stress(ERS)invol ved in the occurrence of atrial fibrillation Method1.Establishment of rat atrial fibrillation model: After fast atrial pacing throug h the esophagus,10 eight-week-old male SD rats were observed to the induced si tuation of atrial fibrillation,and recorded the changes of electrocardiogram before and after the induction of atrial fibrillation.The model of atrial fibrillation group(AF)was prepared,and the control group(control group)was the same as the A F group except for fast atrial pacing through the esophagus.2.Establishment of endoplasmic reticulum stress model in rats and neonatal r at: the rat(adult)cardiomyocytes were stimulated with chlamycin to establish an e ndoplasmic reticulum stress model(group 1),and the neonatal rat cardiomyocytes were stimulated with chlamycin to establish an endoplasmic reticulum stress model(group 2),on which mir-105 was transfected.After mimicking chlamycin + mir-105 mimic group,mouse cardiomyocytes were treated with phosphate buffer solution(PBS)to establish control group 1,neonatal rat cardiomyocytes were treated with phosphate buffer solution(PBS)to establish control group 2,and control group 2was established with mir-105 mimic to establish control group + mir-105 mimic gr oup.3.GRP78 RyR2 and mir-105 detection: phosphorylation levels of glucose-regu lating protein GRP78 RyR2 were detected by protein western blot,and mir-105 in er stress was detected by Real-time PCR after atrial fibrillation.Results1.After rapid atrial pacing through the esophagus in 10 SD rats,After 8 day s,6 atrial fibrillation models were successfully prepared,with n=6 and a success rate of 60%2.Compared with the control group,endoplasmic reticulum stress was activat ed in AF rat heart tissues,GRP 78 expression level was increased(all P < 0.05),RyR2 phosphorylation level was up-regulated(P < 0.05),and mir-105 expression was down-regulated(P < 0.05).3.Compared with control group 1,after atrial myocytes in rats(adult rats)w ere stimulated with chlamycin or isolated with er stress activation(GRP78 express ion up-regulated),mir-105 expression was down-regulated(P < 0.05),RyR2 mRNA and protein expression were up-regulated(P < 0.05),and phosphorylation was in creased(P < 0.05).4.Compared with control group 2,chlamycin stimulated the endoplasmic retic ulum stress activation of newborn rat cardiomyocytes,and the expression level of GRP 78 protein increased(P < 0.05),and the expression of mir-105 was down-re gulated(P < 0.05).On this basis,after transfection with a mir-105 mimic,the ex pression levels of RyR2 mRNA and protein were down-regulated(P < 0.05),and t he phosphorylation level was down-regulated(P < 0.05).Conclusion1.In rat atrial fibrillation model,endoplasmic reticulum stress is activated,Ry R2 expression increases,and phosphorylation expression level increases.2.In the endoplasmic reticulum stress model,the total amount of RyR2 and its phosphorylated expression increased,and the expression of miR-105 decreased,which was negatively correlated.3.MiR-105 has no effect on endoplasmic reticulum stress.4.Endoplasmic reticulum stress is activated during atrial fibrillation.Endoplas mic reticulum stress is involved in the occurrence of atrial fibrillation through the miR-105-RyR2 signaling pathway.